Henrik Wistrand, Niina E Kaartinen, Pekka Jousilahti, Sirpa Jalkanen, Marko Salmi, Teemu Niiranen, Ville Lauri Langén
{"title":"钠摄入量与细胞因子水平之间缺乏关联。","authors":"Henrik Wistrand, Niina E Kaartinen, Pekka Jousilahti, Sirpa Jalkanen, Marko Salmi, Teemu Niiranen, Ville Lauri Langén","doi":"10.2147/IBPC.S483495","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>The complex pathogenesis of hypertension, potentially involving inflammatory pathways, remains elusive. This study aimed to evaluate the relationship between 24-hour urinary sodium excretion and inflammatory cytokines alongside C-reactive protein (CRP) in a nationwide Finnish sample.</p><p><strong>Materials and methods: </strong>265 participants from the FINRISK 2002 study were included in the analyses. Multivariable-adjusted associations of 24-hour urinary sodium with circulating CRP and 26 cytokines were examined.</p><p><strong>Results: </strong>24-hour urinary sodium was not significantly associated with any of the cytokines or CRP (p ≥ 0.02 for all, significance at <0.001). Adjustments for age, sex, serum creatinine concentration, and alcohol intake did not alter these results.</p><p><strong>Conclusion: </strong>This cross-sectional study revealed no associations between 24-hour urinary sodium and cytokine or CRP levels. This does not suggest reducing salt intake would be unbeneficial in hypertension. Additional research is required to clarify the mechanisms through which salt may induce hypertension. Assessing sodium intake in epidemiological studies is also challenging.</p>","PeriodicalId":45299,"journal":{"name":"Integrated Blood Pressure Control","volume":"17 ","pages":"51-57"},"PeriodicalIF":1.5000,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11648537/pdf/","citationCount":"0","resultStr":"{\"title\":\"Lack of Association Between Sodium Intake and Cytokine Levels.\",\"authors\":\"Henrik Wistrand, Niina E Kaartinen, Pekka Jousilahti, Sirpa Jalkanen, Marko Salmi, Teemu Niiranen, Ville Lauri Langén\",\"doi\":\"10.2147/IBPC.S483495\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Purpose: </strong>The complex pathogenesis of hypertension, potentially involving inflammatory pathways, remains elusive. This study aimed to evaluate the relationship between 24-hour urinary sodium excretion and inflammatory cytokines alongside C-reactive protein (CRP) in a nationwide Finnish sample.</p><p><strong>Materials and methods: </strong>265 participants from the FINRISK 2002 study were included in the analyses. Multivariable-adjusted associations of 24-hour urinary sodium with circulating CRP and 26 cytokines were examined.</p><p><strong>Results: </strong>24-hour urinary sodium was not significantly associated with any of the cytokines or CRP (p ≥ 0.02 for all, significance at <0.001). Adjustments for age, sex, serum creatinine concentration, and alcohol intake did not alter these results.</p><p><strong>Conclusion: </strong>This cross-sectional study revealed no associations between 24-hour urinary sodium and cytokine or CRP levels. This does not suggest reducing salt intake would be unbeneficial in hypertension. Additional research is required to clarify the mechanisms through which salt may induce hypertension. Assessing sodium intake in epidemiological studies is also challenging.</p>\",\"PeriodicalId\":45299,\"journal\":{\"name\":\"Integrated Blood Pressure Control\",\"volume\":\"17 \",\"pages\":\"51-57\"},\"PeriodicalIF\":1.5000,\"publicationDate\":\"2024-12-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11648537/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Integrated Blood Pressure Control\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2147/IBPC.S483495\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"PERIPHERAL VASCULAR DISEASE\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Integrated Blood Pressure Control","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2147/IBPC.S483495","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"PERIPHERAL VASCULAR DISEASE","Score":null,"Total":0}
Lack of Association Between Sodium Intake and Cytokine Levels.
Purpose: The complex pathogenesis of hypertension, potentially involving inflammatory pathways, remains elusive. This study aimed to evaluate the relationship between 24-hour urinary sodium excretion and inflammatory cytokines alongside C-reactive protein (CRP) in a nationwide Finnish sample.
Materials and methods: 265 participants from the FINRISK 2002 study were included in the analyses. Multivariable-adjusted associations of 24-hour urinary sodium with circulating CRP and 26 cytokines were examined.
Results: 24-hour urinary sodium was not significantly associated with any of the cytokines or CRP (p ≥ 0.02 for all, significance at <0.001). Adjustments for age, sex, serum creatinine concentration, and alcohol intake did not alter these results.
Conclusion: This cross-sectional study revealed no associations between 24-hour urinary sodium and cytokine or CRP levels. This does not suggest reducing salt intake would be unbeneficial in hypertension. Additional research is required to clarify the mechanisms through which salt may induce hypertension. Assessing sodium intake in epidemiological studies is also challenging.