Encapsulated sodium supplementation of 4weeks does not alter salt taste preferences in a controlled low sodium and low potassium diet

Introduction: We performed a 12-week randomized placebo-controlled crossover study to examine the effects of sodium and potassium supplementation on blood pressure (BP) and arterial stiffness in untreated (pre)hypertensive individuals on a low-sodium, low-potassium diet. Methods: During the study, subjects were on a fully controlled diet that provided on average 2.4 g/d of sodium (equals 6 g/d of salt) and 2.2 g/d of potassium. After a 1-week run-in period, 37 subjects received capsules with supplemental sodium (3 g/d, equals 7.5 g/d of salt), supplemental potassium (3 g/d), or placebo, for four weeks each (not separated by wash-out), in random order. Fasting office BP, 24-h ambulatory BP, and measures of arterial stiffness (SphygmoCor®) were assessed at baseline and after each treatment. Results: Subjects had a mean pre-treatment BP of 145/81 mmHg and 68% (25 of 37) had systolic BP (SBP) ≥140 mmHg. In 36 subjects who completed the study, sodium supplementation increased urinary sodium by 97.6 mmol/24h (2.2 g/d) and potassium supplementation increased urinary potassium by 62.9 mmol/24h (2.5 g/d), compared to placebo (Table). Sodium supplementation significantly increased office BP by 7.5/3.3 mmHg, 24-h BP by 7.0/2.1 mmHg and central BP by 8.5/3.6 mmHg. Potassium supplementation significantly reduced 24-h BP by 4.0/1.7 mmHg. Measures of arterial stiffness did not change. Conclusion: Increasing the intake of sodium has a strong adverse effect on BP in untreated (pre)hypertensive individuals. Increased potassium intake, however, lowers BP even when people are on a reduced sodium diet. Short-term changes in sodium and potassium intake have little effect on arterial stiffness. Trial registration: ClinicalTrials.gov Identifier: NCT01575041

Download Full-text

Repeated Exposure to Low-Sodium Cereal Affects Acceptance but Does not Shift Taste Preferences or Detection Thresholds of Children in a Randomized Clinical Trial

Journal of Nutrition ◽

10.1093/jn/nxz014 ◽

2019 ◽

Vol 149 (5) ◽

pp. 870-876 ◽

Cited By ~ 2

Author(s):

Nuala Bobowski ◽

Julie A Mennella

Keyword(s):

Repeated Measures ◽

Salt Intake ◽

Energy Content ◽

Sodium Intake ◽

Dietary Sodium ◽

Taste Preferences ◽

Detection Thresholds ◽

Salt Taste ◽

Low Sodium ◽

Secondary Outcomes

ABSTRACT Background Although salt taste preference is malleable in adults, no research to date has focused on children, whose dietary sodium intake exceeds recommended intake and whose salt taste preferences are elevated. Objective This proof-of-principle trial determined whether 8-wk exposure to low-sodium cereal (LSC) increased children's acceptance of its taste and changed their salty and sweet taste preferences. Methods Children (n = 39; ages 6–14 y; 67% female) were randomly assigned to ingest LSC or regular-sodium cereal (RSC) 4 times/wk for 8 wk. The cereals, similar in sugar (3 g/cup compared with 2 g/cup) and energy content (100 kcal/cup) yet different in sodium content (200 mg sodium/cup compared with 64 mg sodium/cup), were chosen based on taste evaluation by a panel of children. Mothers completed daily logs on children's cereal intake. At baseline and after the exposure period, taste tests determined which cereal children preferred and measured children's most preferred amount of salt (primary outcomes), and most preferred amount of sucrose and salt taste detection thresholds (secondary outcomes). Repeated measures ANOVAs were conducted on primary and secondary outcomes, and generalized estimating equations were conducted on amount of cereal ingested at home over time. Results Both treatment groups accepted and ate the assigned cereal throughout the 8-wk exposure. There were no group × time interactions in salt detection thresholds (P = 0.32) or amount of salt (P = 0.30) and sucrose (P = 0.77) most preferred, which were positively correlated (P = 0.001). At baseline and after the exposure, the majority in both groups preferred the taste of the RSC relative to LSC (P > 0.40). Conclusions Children showed no change in salt preference but readily ate the LSC for 8 consecutive weeks. Findings highlight the potential for reducing children's dietary salt intake by incorporating low-sodium foods in the home environment without more preferred higher-salt versions of these foods. This trial was registered at clinicaltrials.gov as NCT02909764.

Download Full-text

Effect of a 6-month Low Sodium Diet on the Salt Taste Perception and Pleasantness, Blood Pressure and the Urinary Sodium Excretion in Female College Students

The Korean Journal of Nutrition ◽

10.4163/kjn.2010.43.5.433 ◽

2010 ◽

Vol 43 (5) ◽

pp. 433 ◽

Cited By ~ 16

Author(s):

Soon-Ok Chang

Keyword(s):

College Students ◽

Blood Pressure ◽

Sodium Excretion ◽

Urinary Sodium Excretion ◽

Taste Perception ◽

Female College Students ◽

Female College ◽

Salt Taste ◽

Low Sodium Diet ◽

Low Sodium

Download Full-text

Response of tissue electrolytes to respiratory acidosis

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1961.200.6.1151 ◽

1961 ◽

Vol 200 (6) ◽

pp. 1151-1154 ◽

Cited By ~ 4

Author(s):

Howard Levitin ◽

Carol J. Amick ◽

Franklin H. Epstein

Keyword(s):

Metabolic Acidosis ◽

Respiratory Acidosis ◽

Calcium Content ◽

Normal Diet ◽

Electrolyte Composition ◽

Low Sodium Diet ◽

Low Sodium ◽

Low Potassium ◽

Low Levels ◽

Sodium And Potassium

The effect of 8% CO2 for 24 hr on the electrolyte composition of muscle, bone, and liver has been studied in rats on a normal diet as well as on one low in sodium and low in potassium. Muscle potassium decreased in animals on a normal or low-sodium diet exposed to CO2. Muscle sodium decreased in animals on a low-potassium diet exposed to CO2, and there was no further change in the already low levels of muscle potassium. The sodium and potassium content of bone and liver and the calcium content of bone were unchanged by exposure to CO2. Nephrectomy blocks the loss of muscle potassium noted in rats on a normal diet. Muscle and bone sodium were also unaltered by CO2 in nephrectomized rats. These results contrast with those obtained during metabolic acidosis and emphasize the importance of the kidneys in bodily adjustments to respiratory acidosis.

Download Full-text

Systematic review and meta-analysis of risk factor for postoperative delirium following spinal surgery

Journal of Orthopaedic Surgery and Research ◽

10.1186/s13018-020-02035-4 ◽

2020 ◽

Vol 15 (1) ◽

Author(s):

Hao Jie Zhang ◽

Xue Hai Ma ◽

Jin Biao Ye ◽

Cong Zhi Liu ◽

Zhi Yang Zhou

Keyword(s):

Risk Factors ◽

Spinal Surgery ◽

Postoperative Delirium ◽

Meta Analysis ◽

Operating Time ◽

Economic Costs ◽

Total Blood ◽

Low Sodium ◽

Low Potassium ◽

History Of

Abstract Background Postoperative delirium is a common psychiatric disorder among patients who undergo spinal surgery. The purpose of current meta-analysis was to assess the potential risk factors related to delirium in spinal surgery. Methods We searched the following databases: PubMed, EMBASE, the Cochrane Library, and Web of Science, from inception to July 2020. Two reviewers independently assessed the quality of the included studies using the previously described Newcastle-Ottawa Scale (NOS). We included spinal surgery patients who suffered with delirium or not. Stata 12.0 was used for meta-analysis. Results Thirteen trial studies that met our inclusion criteria were incorporated into the meta-analysis. Postoperative delirium was associated with an increase of the duration of hospital stay (P = 0.044) and increased perioperative readmission rate (P = 0.013) and economic costs (P = 0.002). This meta-analysis demonstrates that there were twenty-two risk factors: general characteristic: old age, female patients, history of surgery, diabetes mellitus, hypertension; preoperative data: low hematocrit, low hemoglobin, low albumin, low sodium, depression; operative data: operating time, total blood loss; postoperative data: low sodium, low hemoglobin, low hematocrit, low albumin, fever, low potassium, blood sugar, and visual analog scale (VAS). Conclusions Delirium not only prolongs the length of hospital stay, but also increases readmission rate and the economic costs. Several risk factors including old age, female patients, history of surgery, diabetes mellitus, low hematocrit, low hemoglobin, low albumin, low sodium, depression; operative data: operating time, total blood loss, low sodium, low hemoglobin, low hematocrit, low albumin, fever, low potassium, blood sugar, and VAS were significant predictors for postoperative delirium after spinal surgery.

Download Full-text

Pressor resistance to vasopressin in sodium depletion, potassium depletion, and cirrhosis

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1986.251.3.r525 ◽

1986 ◽

Vol 251 (3) ◽

pp. R525-R530 ◽

Cited By ~ 3

Author(s):

B. M. Murray ◽

M. S. Paller

Keyword(s):

Pressor Response ◽

Potassium Depletion ◽

Pressor Effect ◽

Sodium Depletion ◽

Sprague Dawley ◽

Low Sodium Diet ◽

Low Sodium ◽

Sprague Dawley Rats ◽

Low Potassium ◽

Baroreceptor Reflexes

Resistance to the pressor effects of angiotensin II, but not norepinephrine, has been observed in sodium depletion, potassium depletion, and cirrhosis. We tested the response to arginine vasopressin (AVP) in each of these conditions. Male Sprague-Dawley rats were made sodium depleted with furosemide and a low-sodium diet for 3 days, potassium depleted by feeding a low-potassium diet for 14-21 days, or cirrhotic by inhalation of carbon tetrachloride for 8 wk. In conscious rats, the pressor response to graded doses of AVP was reduced in sodium depletion by 27-43% compared with control rats. Sodium-depleted rats were also found to have enhanced baroreceptor reflexes, since the decrease in heart rate for a given increase in mean arterial pressure was greater than in control rats. When the ganglionic blocker pentolinium tartrate was given to sodium-depleted rats the pressor response to AVP was restored to control levels. In potassium-depleted rats the pressor response to AVP was 21-52% lower than that in controls, whereas cirrhotic rats also had a blunted response to AVP (14-41% lower than control). However, there was no evidence in either of these two states of enhanced baroreceptor activity, and pretreatment with pentolinium tartrate did not restore the pressor response to normal. Therefore, although resistance to the pressor effect of AVP was found in all three conditions, the mechanism of this effect was different in sodium depletion compared with potassium depletion and cirrhosis. We conclude that resistance to the pressor action of AVP in sodium depletion was secondary to resetting of the baroreceptors.

Download Full-text