Lysine and salt-sensitive hypertension.

PURPOSE OF REVIEW: Salt-sensitive (SS) hypertension and its associated kidney damage have been extensively studied, yet proper therapeutic strategies are lacking. The interest in altering the metabolome to affect renal and cardiovascular disease has been emerging. Here, we discuss the effect and potential mechanism behind the protective effect of lysine, an essential amino acid, on the progression of SS hypertension. RECENT FINDINGS: We have recently demonstrated that administering lysine in an SS rodent model can control the progression of hypertension. Both the animal and pilot human studies showed that lysine can efficiently inhibit tubular reabsorption of albumin and protect the kidneys from further damage. In addition, we conducted multilevel omics studies that showed increased lysine conjugation and excretion, leading to the depletion of harmful metabolites and an increase in useful ones. SUMMARY: Lysine's twofold action involves both mechanically flushing protein from proximal tubules to shield the kidneys and initiating metabolic adaptations in the kidneys. This results in a net positive impact on SS hypertension. While further research is necessary to apply the current findings in clinical settings, this study offers some evidence suggesting that lysine supplementation holds promise as a therapeutic approach for hypertensive kidney disease.

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.

Potassium-Enriched Salt Substitutes: A Review of Recommendations in Clinical Management Guidelines.

Excess dietary sodium intake and insufficient dietary potassium intake are both well-established risk factors for hypertension. Despite some successful initiatives, efforts to control hypertension by improving dietary intake have largely failed because the changes required are mostly too hard to implement. Consistent recent data from randomized controlled trials show that potassium-enriched, sodium-reduced salt substitutes are an effective option for improving consumption levels and reducing blood pressure and the rates of cardiovascular events and deaths. Yet, salt substitutes are inconsistently recommended and rarely used. We sought to define the extent to which evidence about the likely benefits and harms of potassium-enriched salt substitutes has been incorporated into clinical management by systematically searching guidelines for the management of hypertension or chronic kidney disease. We found incomplete and inconsistent recommendations about the use of potassium-enriched salt substitutes in the 32 hypertension and 14 kidney guidelines that we reviewed. Discussion among the authors identified the possibility of updating clinical guidelines to provide consistent advice about the use of potassium-enriched salt for hypertension control. Draft wording was chosen to commence debate and progress consensus building: strong recommendation for patients with hypertension-potassium-enriched salt with a composition of 75% sodium chloride and 25% potassium chloride should be recommended to all patients with hypertension, unless they have advanced kidney disease, are using a potassium supplement, are using a potassium-sparing diuretic, or have another contraindication. We strongly encourage clinical guideline bodies to review their recommendations about the use of potassium-enriched salt substitutes at the earliest opportunity.

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.

Oat Peptides Alleviate Dextran Sulfate Sodium Salt-Induced Colitis by Maintaining the Intestinal Barrier and Modulating the Keap1-Nrf2 Axis.

The prevalence of inflammatory bowel disease (IBD) is progressively rising each year, emphasizing the significance of implementing rational dietary interventions for disease prevention. Oats, being a staple agricultural product, are abundant in protein content. This study aimed to investigate the protective effects and underlying mechanisms of oat peptides (OPs) in a mouse model of acute colitis induced by dextran sulfate sodium salt (DSS) and a Caco-2 cell model. The findings demonstrated that intervention with OPs effectively mitigated the symptoms associated with DSS-induced colitis. The physicochemical characterization analysis demonstrated that the molecular weight of the OPs was predominantly below 5 kDa, with a predominant composition of 266 peptides. This study provides further evidence of the regulatory impact of OPs on the Keap1-Nrf2 signaling axis and elucidates the potential role of WGVGVRAERDA as the primary bioactive peptide responsible for the functional effects of OPs. Ultimately, the results of this investigation demonstrate that OPs effectively mitigate DSS-induced colitis by preserving the integrity of the intestinal barrier and modulating the Keap1-Nrf2 axis. Consequently, these findings establish a theoretical foundation for the utilization of OPs as dietary supplements to prevent the onset of IBD.

Soy Sauce Lowers Body Weight and Fat Mass in High-Fat Diet-Induced Obese Rats.

Soy sauce (SS) is a traditional fermented seasoning. Although fermented foods have diverse health beneficial effects, SS intake has been discouraged because of its high salt level. This study was designed to evaluate the antiobesity outcomes of SS and the potential involvement of salt content in SS by adding a high-salt group. Sprague-Dawley rats were randomly assigned into four groups: normal diet (ND, 10% fat of total kcal), high-fat diet (HD, 60% fat of total kcal), HD with salt water (HDSW, NaCl = 8%), and HD with SS (HDSS, NaCl = 8%). SS significantly decreased HD-induced body weight gain and lipogenic gene expression without affecting food consumption. Moreover, SS also reduced hepatic injury and lipid accumulation, and also improved hyperlipidemia. Furthermore, SS decreased the mRNA levels related to obesity-derived inflammatory responses, while HDSW did not change the levels of those markers. These observations indicate that SS ameliorates obesity in HD-fed obese rats by attenuating dyslipidemia. Moreover, SS might also have an anti-inflammatory effect in HD-induced obesity, which requires further investigation. Most importantly, SS offers these beneficial effects regardless of its high salt content, implying that different dietary salt sources lead to the distinct health outcomes. In conclusion, the findings of this study improve the understanding of the functional effect of SS.

Effectiveness of a community health worker-led low-sodium salt intervention to reduce blood pressure in rural Bangladesh: protocol for a cluster randomized controlled trial.

BACKGROUND: High blood pressure is a major public health problem in low- and middle-income countries. Low-sodium salt substitute (LSSS) is a promising population-level blood pressure-lowering intervention requiring minimal behavioral change. The optimal method of delivering LSSS to individuals, however, is currently unknown. Community health workers (CHWs) have successfully been used to implement health interventions in Bangladesh and may provide a venue for the dissemination of LSSS. METHODS: We aim to conduct a cluster-randomized controlled trial involving 309 households in rural Bangladesh previously identified and characterized by the BRAC James P Grant School of Public Health, BRAC University (BRAC JPGSPH). These households will be randomly assigned to three arms: (1) control, i.e., no intervention; (2) information only, i.e., community health workers will provide basic information on high blood pressure, the health consequences of excessive salt consumption, and feedback to the participant on the likely quantity of salt s/he consumes (estimated using a questionnaire); (3) free LSSS arm: the same information as in arm 2 will be provided, but participants will receive 6 months of free low-sodium salt along with education on the benefits of LSSS. One male and one female adult (age ≥ 18 years) in each household will be invited to participate, the exclusion criteria being households with members known to have high serum potassium levels, are taking medications known to elevate potassium levels (e.g., ACE inhibitors, ARBs, potassium-sparing diuretics), are already taking potassium supplements, or those who have known kidney disease or abnormal serum creatinine at baseline. The primary endpoint will be blood pressure at 6 months post-intervention. DISCUSSION: Recent large clinical trials of LSSS in China and India have shown not only blood pressure improvements, but also stroke, major cardiac event, and all-cause mortality reductions. Nevertheless, how to best translate this intervention to population-level effectiveness remains unclear. Our study would test whether a community health worker-based program could be effectively used to disseminate LSSS and achieve measurable blood pressure benefits. TRIAL REGISTRATION: ClinicalTrials.gov NCT05425030. Registered on June 21, 2022.

Less sodium, more potassium, or both: population-wide strategies to prevent hypertension.

Hypertension is among the most prevalent medical conditions globally and a major contributor to chronic kidney disease, cardiovascular disease, and death. Prevention through nonpharmacological, population-level interventions is critically needed to halt this worldwide epidemic. However, there are ongoing disagreements as to where public policy efforts should focus. Recently the Salt Substitute and Stroke Study demonstrated the efficacy of substituting table salt with potassium salt to reduce the risk of stroke, major cardiovascular events, and death. However, this sparked debate over whether sodium or potassium should be prioritized in countries where table salt substitution was less feasible. In this commentary, we summarize arguments in favor of either strategy: reduced sodium or increased potassium intake. Moreover, we discuss evidence and policy approaches related to either or combined approaches relevant to cultural context. Ultimately, there is an urgent need for policies that both reduce sodium and increase potassium intake; however, identifying a strategy that fits cultural context will be key to improve population-wide blood pressures.

Metabolomics reveals the defense mechanism of histidine supplementation on high-salt exposure-induced hepatic oxidative stress.

AIMS: This study mainly evaluated the protective mechanism of histidine against the hepatic oxidative stress after high-salt exposure (HSE) through combined analysis of non-targeted metabolomics and biological metabolic networks. MATERIALS AND METHODS: Dahl salt-sensitive (SS) rats were fed with normal-salt diet or HSE ± histidine in addition to drinking water for 14 days. Gas chromatography-mass spectrometry was used to analyze the hepatic metabolites. The metabolic profile was analyzed by SIMCA-14.1, the metabolic correlation network was performed using Gephi-0.9.2, and pathway enrichment was analyzed using MetaboAnalyst 5.0 online website. KEY FINDINGS: Results indicated that HSE disturbed the hepatic metabolic profile, generated abnormal liver metabolism and exacerbated oxidative stress. Histidine supplementation significantly reversed the hepatic metabolic profile. Of note, 14 differential metabolic pathways were enriched after histidine supplementation, most of which played an important role in ameliorating redox and nitric oxide (NO) metabolism. Histidine administration decreased the levels of hydroperoxide and malondialdehyde, and increased the activities of antioxidant enzymes (Catalase, Superoxide Dismutase, Glutathione S-transferase and Glutathione reductases). Histidine effectively enhanced the endogenous synthesis of glutathione by increasing the levels of glutamate and cysteine, thereby enhancing the antioxidant capacity of the glutathione system. After histidine administration, lysine, glutamate, and hypotaurine owned a higher metabolic centrality in the correlation network. In addition, histidine could also effectively increase the endogenous synthesis of NO by enhancing the L-arginine/NO pathway. SIGNIFICANCE: This study offers new insights into the metabolic mechanisms underlying the antioxidant protective effect of histidine on the liver.

Implementation of non-pharmacological interventions for the treatment of hypertension in primary care: a narrative review of effectiveness, cost-effectiveness, barriers, and facilitators.

BACKGROUND: The current guidelines for the prevention, detection, evaluation, and management of hypertension recommend six types of non-pharmacological interventions: alcohol reduction, salt intake reduction, increased potassium intake, physical activity, weight loss, and heart-healthy diets. However, the non-pharmacological interventions are still not widely used in primary care. In this paper, we, therefore, reviewed and summarised the evidence on the effectiveness, cost-effectiveness, barriers, and facilitators of non-pharmacological interventions for the treatment of hypertension in primary care. METHODS: A thorough literature search was conducted in Embase, Google Scholar, and PubMed databases, to identify the most recent reviews or, in their absence, primary studies on alcohol reduction, salt intake reduction, potassium supplementation, physical activity, weight reduction, heart-healthy diets, and other non-pharmacological interventions for the treatment of hypertension in primary care. RESULTS: Alcohol reduction is a non-pharmacological intervention for the treatment of hypertension in primary care with proven effectiveness, feasibility, and acceptability. Interventions for sodium intake reduction, physical activity, and weight reduction are effective but there is insufficient evidence regarding their feasibility and acceptability in primary care settings. Evidence on the effectiveness of potassium intake and heart-healthy diets is limited and inconsistent. There is a lack of evidence on the cost-effectiveness of non-pharmacological interventions in the treatment of hypertension. The most common barriers to deliver such interventions related to healthcare providers include a lack of time, knowledge, self-confidence, resources, clear guidelines, and financial incentives. The most common barriers related to patients include a lack of motivation and educational resources. Less evidence is available on facilitators of implementing non-pharmacological interventions in primary care. Besides, facilitators differed by different types of interventions. CONCLUSIONS: Available evidence suggests that more pragmatic, clinically feasible, and logistically simple interventions are required for sodium intake reduction, physical activity, and weight reduction in primary care settings. Future studies should provide further evidence on the effectiveness of weight control, potassium intake, and heart-healthy diets. More research is also needed on cost-effectiveness and facilitators of all types of effective non-pharmacological interventions for the treatment of hypertension in primary care.

[Can salt substitution or reduction replace pharmaceuticals for arterial hypertension?] / Kann eine Salzsubstitution oder -reduktion bei arterieller Hypertonie Arzneimittel ersetzen?

Nonpharmacological treatment is still an important supplement to the pharmacological treatment of hypertension. Thereby, either an elevated blood pressure can be lowered further or, alternatively, the use of antihypertensive drugs can be reduced. In the context of nonpharmacological treatment of hypertension, sodium restriction plays an important role. Sodium intake can either be reduced by lowering excessive dietary salt consumption or by the use of table salts with reduced sodium content. Lower dietary sodium consumption lowers blood pressure. This was controversial for a long time; however, now more and more observational and interventional studies have confirmed this fact. Nevertheless, some studies have shown an association of low salt consumption with increased mortality. This observation is explained by the so-called reverse epidemiology. This means that diseases with increased mortality, such as consuming diseases or severe heart diseases are associated with lowered food intake and as a consequence, with lower sodium intake. In addition to sodium restriction, the use of so-called salt substitutes with lower sodium content is also effective in lowering blood pressure. In most of the salt substitutes examined so far sodium chloride is partly replaced by potassium chloride. Numerous investigations show that these salt substitutes lower blood pressure. From a statistical point of view side effects such as hyperkalemia are very rare; however, hyperkalemia is potentially life-threatening. Therefore, the broader use of these salt substitutes is principally helpful but these salts should only be used after medical consultation. Especially renal insufficiency and the use of certain drugs, such as potassium-sparing diuretics and blockers of the renin-angiotensin system increase the risk of hyperkalemia.

Momordica charantia Extract Confers Protection Against Hypertension in Dahl Salt-Sensitive Rats.

Hypertension is one of the main factors of cardiovascular disease worldwide and is strongly related to the overall mortality. High salt intake is a major risk factors for hypertension. Identifying functional foods that can help prevent mechanistic abnormalities mediating salt-induced hypertension is an issue of considerable nutraceutical and scientific interest. Dietary Momordica charantia may be an alternative approach to avoid salt-induced hypertension. Dahl salt-sensitive (DSS) rats were used to determine whether Momordica charantia water extracts (ME) exerts anti-hypertensive effects in the present study. ME gavage could significantly prevented the increase of blood pressure, blood urea nitrogen, creatinine, and urine protein-to-creatinine ratio of DSS rats. Metabolomics analysis indicated that high-salt diet induced abnormal amino acid metabolism was related to nitric oxide (NO) deficiency, but ME gavage could upregulate the activities of nitric oxide synthase, aspartate aminotransferase, argininosuccinate lyase, argininosuccinate synthase and restore endogenous synthesis of arginine and NO. Meanwhile, renal function was improved after ME gavage. Citrulline, as one of the important component in ME, could attenuate salt-induced hypertension by increasing endogenous synthesis of arginine and NO. Antioxidants in ME, such as phenolic compound, may avoid high-salt induced oxidative stress in DSS rats, which may be another mechanism by which ME prevented blood pressure increase. Thus, the present study indicated that feeding Momordica charantia could avoid high-salt-induced hypertension in DSS rats.

The Impact of Iodine Concentration Disorders on Health and Cancer.

Iodine deficiency is an ongoing problem. The implementation of salt iodization has significantly reduced the effects of iodine deficiency worldwide in recent years, and the remaining iodine deficiency is mild to moderate. Iodine is an essential substrate for the synthesis of thyroid hormones in the thyroid gland. It can also act as an antioxidant, as well as an anti-proliferative and pro-apoptotic factor. Pregnant women, breastfeeding women, and children are particularly affected by iodine deficiency. It leads to thyroid diseases and metabolic and developmental disorders, as well as cancer. However, an excessive iodine intake may, similarly to iodine deficiency, lead to the development of goiter, and toxic amounts of iodine can lead to thyroiditis, hyperthyroidism, and hypothyroidism, and even to the development of papillary thyroid cancer. Correcting iodine deficiency potentially reduces the chance of developing malignancies. Additional research is needed to better understand both the effect of iodine on carcinogenesis and the clinical outcome of iodine deficiency compensation on cancer patients' prognosis. The upcoming public health challenge appears to be reducing salt consumption, which could result in a lower iodine intake. Thus, an iodine enrichment vehicle other than salt could be considered if salt iodine levels are not increased to compensate, and urine iodine levels should be monitored more frequently.

The Effect of Diet on Cardiovascular Disease, Heart Disease, and Blood Vessels.

The Effect of Diet on Cardiovascular Disease, Heart Disease, and Blood Vessels [...].

Protective Effect of Gamma Aminobutyric Acid against Aggravation of Renal Injury Caused by High Salt Intake in Cisplatin-Induced Nephrotoxicity.

Gamma-aminobutyric acid (GABA) is one of the inhibitory neurotransmitters. Several studies have suggested that GABA supplements can reduce blood pressure and modulate the renal immune system in vitro and in vivo. In the present study, we investigated the effect of GABA-enriched salt as an alternative to traditional salt on aggravated renal injury by high salt intake in cisplatin-induced nephrotoxicity mice. High salt intake accelerated the increase of biomarkers, such as blood urea nitrogen and serum creatinine levels for renal injury in cisplatin-induced nephrotoxicity mice. However, oral administration of GABA-contained salt notably suppressed serum BUN and creatinine levels. The efficacy of GABA salt was superior to lacto GABA salt and postbiotics GABA salt. Furthermore, GABA-enriched salt markedly restored histological symptoms of nephrotoxicity including renal hypertrophy, tubular dilation, hemorrhage, and collagen deposition aggravated by salt over-loading in cisplatin-exposed mice. Among them, GABA salt showed a higher protective effect against cisplatin-induced renal histological changes than lacto GABA salt and postbiotics GABA salt. In addition, administration of high salt significantly enhanced expression levels of apoptosis and inflammatory mediators in cisplatin-induced nephrotoxicity mice, while GABA-enriched salt greatly down-regulated the expression of these mediators. Taken together, these results demonstrate the protective effect of GABA against damage caused by high salt intake in cisplatin-induced renal toxicity. Its mechanism may be due to the suppression of hematological and biochemical toxicity, apoptosis, and inflammation. In conclusion, although the protective efficacy of GABA salt on renal injury is different depending on the sterilization and filtration process after fermentation with L. brevis BJ20 and L. plantarum BJ21, our findings suggest that GABA-enriched salt has a beneficial effect against immoderate high salt intake-mediated kidney injury in patients with cisplatin-induced nephrotoxicity.

Supplementation of amino acids and organic acids prevents the increase in blood pressure induced by high salt in Dahl salt-sensitive rats.

A high-salt (HS) diet leads to metabolic disorders in Dahl salt-sensitive (SS) rats, and promotes the development of hypertension. According to the changes in the metabolites of SS rats, a set of combined dietary supplements containing amino acids and organic acids (AO) were designed. The purpose of the present study was to evaluate the effect of AO supplementation on the blood pressure of SS rats after the HS diet and clarify the mechanism of AO by metabolomics and biochemical analyses. The results showed that AO supplementation avoided the elevation of blood pressure induced by the HS diet in SS rats, increased the renal antioxidant enzyme activities (catalase, superoxide dismutase, glutathione reductase, and glutathione S-transferase), reduced the H2O2 and MDA levels, and restored the normal antioxidant status of the serum and kidneys. AO also reversed the decrease in the nitric oxide (NO) levels and NO synthase activity induced by the HS feed, which involved the L-arginine/NO pathway. Metabolomics analysis showed that AO administration increased the levels of amino acids such as cysteine, glycine, hypotaurine, and lysine in the renal medulla and the levels of leucine, isoleucine, and serine in the renal cortex. Of note, lysine, hypotaurine and glycine had higher metabolic centrality in the metabolic correlation network of the renal medulla after AO administration. In conclusion, AO intervention could prevent HS diet-induced hypertension in SS rats by restoring the metabolic homeostasis of the kidneys. Hence, AO has the potential to become a functional food additive to improve salt-sensitive hypertension.

Calcitriol ameliorates damage in high-salt diet-induced hypertension: Evidence of communication with the gut-kidney axis.

Several studies have established a link between high-salt diet, inflammation, and hypertension. Vitamin D supplementation has shown anti-inflammatory effects in many diseases; gut microbiota is also associated with a wide variety of cardiovascular diseases, but potential role of vitamin D and gut microbiota in high-salt diet-induced hypertension remains unclear. Therefore, we used rats with hypertension induced by a high-salt diet as the research object and analyzed the transcriptome of their tissues (kidney and colon) and gut microbiome to conduct an overall analysis of the gut-kidney axis. We aimed to confirm the effects of high salt and calcitriol on the gut-kidney immune system and the composition of the intestinal flora. We demonstrate that consumption of a high-salt diet results in hypertension and inflammation in the colon and kidney and alteration of gut microbiota composition and function. High-salt diet-induced hypertension was found to be associated with seven microbial taxa and mainly associated with reduced production of the protective short-chain fatty acid butyrate. Calcitriol can reduce colon and kidney inflammation, and there are gene expression changes consistent with restored intestinal barrier function. The protective effect of calcitriol may be mediated indirectly by immunological properties. Additionally, the molecular pathways of the gut microbiota-mediated blood pressure regulation may be related to circadian rhythm signals, which needs to be further investigated. An innovative association analysis of the microbiota may be a key strategy to understanding the association between gene patterns and host.

Effects of almonds on ameliorating salt-induced hypertension in dahl salt-sensitive rats.

BACKGROUND: Excessive dietary salt intake is related to an increased risk of hypertension. Dietary functional foods probably could help to improve salt-induced hypertension. In this study, Dahl salt-sensitive (DSS) rats were used to investigate their metabolic differences from those of salt-resistant SS.13BN rats and determine whether dietary protein-rich almonds could ameliorate salt-induced elevation of blood pressure in DSS rats. RESULTS: After high-salt intake, the systolic blood pressure and mean arterial pressure of the DSS rats increased dramatically. Metabolomics analysis indicated abnormal amino acid metabolism in their kidneys. Their renal nitric oxide (NO) content and nitric oxide synthase activity decreased significantly after high-salt diet. Oxidative stress also occurred in DSS rats. After the DSS rats received almond supplementation, the levels of various amino acids in their kidney increased, and renal arginine and NO contents were upregulated. Their renal hydrogen peroxide and malonaldehyde levels decreased, whereas renal catalase, superoxide dismutase and glutathione peroxidase activities and glutathione levels increased. CONCLUSION: The renal abnormal amino acid metabolism of DSS rats contributed to the impaired NO production in response to high-salt intake. Together with salt-induced oxidative stress, high-salt diet intake ultimately led to an increase in the blood pressure of DSS rats. Protein-rich almond supplementation might prevent the development of salt-induced hypertension by restoring arginine and NO regeneration and alleviating salt-induced oxidative stress. © 2021 Society of Chemical Industry.

Association of Estimated Salt and Miso Intake with the Prevalence of Obesity in People with Type 2 Diabetes: A Cross-Sectional Study.

Salt intake is often estimated by the amount of sodium excreted in urine, and miso has been reported to increase it. This cross-sectional study investigated the relationship between obesity and high estimated salt intake with and without habitual miso consumption. Estimates of salt intake (g/day) were calculated using urinary sodium excretion, and a high estimated intake was defined as greater than the median amount of 9.5 g/day. Participants were divided into four groups based on estimated salt intake and miso consumption. Among 300 people, the proportions of obesity were 77.8% (n = 14/18), 40.2% (n = 53/132), 26.0% (n = 33/127), and 34.8% (n = 8/23) in the (+/-), (+/+), (-/+), and (-/-) groups of high estimated salt intake/habitual miso consumption, respectively. Compared with the (+/-) group, the adjusted odds ratios for obesity were 0.07 (95% confidence interval (CI): 0.02-0.26, p < 0.001), 0.16 (95% CI: 0.03-0.76, p = 0.022), and 0.14 (95% CI: 0.04-0.51, p = 0.003) in the (-/+), (-/-), and (+/+) groups, respectively. The presence of obesity was not much higher in people with high estimated salt intake with habitual miso consumption than that in people without. Clinicians should be aware that miso consumption promotes salt excretion, which may lead to an apparently higher estimated salt intake than actual.

Iodine monitoring models contribute to avoid adverse birth outcomes related more than adequate iodine intake.

BACKGROUND: Iodine plays an important role in pregnancy. How to maintain adequate iodine intake amongst pregnant women in each trimester of pregnancy to prevent adverse birth outcomes in central China is a challenge for clinical practice. METHODS: 870 pregnant women and their infants were enrolled in the study. Urinary iodine concentration (UIC) was measured using an inductively coupled plasma mass spectrometry (ICP-MS). Maternal and newborn information were obtained during follow-up. Multinomial logistic regression models were established. RESULTS: Median UIC of pregnant women was 172 ± 135 µg/L which is currently considered to be sufficient. Multivitamin supplements containing iodine, iodized salt intake and frequent milk intake were significantly associated with higher UIC. Multivariate logistic regression analysis showed that multivitamin supplements containing iodine and milk consumption were risk factors for more than adequate iodine (UIC ≥ 250 µg/L). Iodine-rich diet was significantly related to heavier birthweight, larger head circumference and longer femur length of the newborns while more than adequate iodine intake (UIC ≥ 250 µg/L) was a risk factor for macrosomia. Logistic regression models based on potential risk factors involving iodine containing supplements and iodine-rich diet were established to predict and screen pregnant women with high risk of more than adequate iodine intake among local pregnant women in different trimesters and guide them to supplement iodine reasonably to prevent the risk. CONCLUSIONS: Multivitamin supplements containing iodine and milk consumption were risk factors for maternal UIC ≥ 250 µg/L which was a risk factor for macrosomia. Iodine monitoring models were established to provide guidance for pregnant women to reduce the risk of more than adequate iodine intake, thereby contributing to reduce the risk of having a macrosomia.