{"title":"我们应该摄入多少钠?","authors":"Chen Shen, P. J. Bowers, Y. Bar-Yam","doi":"10.1097/pp9.0000000000000026","DOIUrl":null,"url":null,"abstract":"Introduction: Sodium, an important dietary requirement, is essential to many physiologic processes. High sodium intake affects serious health issues such as hypertension and cardiovascular disease, the largest cause of death globally. Consequently, many health organizations have recommended substantial reductions in sodium intake, to as little as 1,500 mg/d. Yet limited understanding exists for the entire range of the effect of sodium between high intake and the recommendations. Methods: We built a simulation using equations from the Uttamsingh model of the renal system to simulate the long-term mean arterial pressure (MAP) across sodium intake ranges. We used another existing physiology simulation platform, HumMod-3.0.4, for comparison. We compared the simulation results with empirical studies done on the global population. Results: We find a linear increase in MAP for consumption above 4,000 mg/d, but nearly constant MAP between 1,200 and 4,000 mg/d. Below 1,200 mg/d, the system cannot maintain homeostasis. Conclusion: Supporting the U-shape theory of sodium intake, which posits that too-high and too-low sodium intake rates increase cardiovascular disease risks, our results suggest that the homeostatic regulation by antidiuretic hormone and aldosterone transitions from sodium retention to sodium excretion at around 4,000 mg/d (a value that varies across individuals and conditions), indicating sodium saturation and evolutionary optimality. Our findings are consistent with recent empirical studies on large populations globally. We suggest that the current low-level recommendations are not supported by this physiologic model analysis and would require more compelling evidence.","PeriodicalId":92284,"journal":{"name":"Progress in preventive medicine (New York, N.Y.)","volume":"5 1","pages":"e0026"},"PeriodicalIF":0.0000,"publicationDate":"2019-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/pp9.0000000000000026","citationCount":"0","resultStr":"{\"title\":\"How Much Sodium Should We Eat?\",\"authors\":\"Chen Shen, P. J. Bowers, Y. Bar-Yam\",\"doi\":\"10.1097/pp9.0000000000000026\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Introduction: Sodium, an important dietary requirement, is essential to many physiologic processes. High sodium intake affects serious health issues such as hypertension and cardiovascular disease, the largest cause of death globally. Consequently, many health organizations have recommended substantial reductions in sodium intake, to as little as 1,500 mg/d. Yet limited understanding exists for the entire range of the effect of sodium between high intake and the recommendations. Methods: We built a simulation using equations from the Uttamsingh model of the renal system to simulate the long-term mean arterial pressure (MAP) across sodium intake ranges. We used another existing physiology simulation platform, HumMod-3.0.4, for comparison. We compared the simulation results with empirical studies done on the global population. Results: We find a linear increase in MAP for consumption above 4,000 mg/d, but nearly constant MAP between 1,200 and 4,000 mg/d. Below 1,200 mg/d, the system cannot maintain homeostasis. Conclusion: Supporting the U-shape theory of sodium intake, which posits that too-high and too-low sodium intake rates increase cardiovascular disease risks, our results suggest that the homeostatic regulation by antidiuretic hormone and aldosterone transitions from sodium retention to sodium excretion at around 4,000 mg/d (a value that varies across individuals and conditions), indicating sodium saturation and evolutionary optimality. Our findings are consistent with recent empirical studies on large populations globally. We suggest that the current low-level recommendations are not supported by this physiologic model analysis and would require more compelling evidence.\",\"PeriodicalId\":92284,\"journal\":{\"name\":\"Progress in preventive medicine (New York, N.Y.)\",\"volume\":\"5 1\",\"pages\":\"e0026\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2019-12-26\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1097/pp9.0000000000000026\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Progress in preventive medicine (New York, N.Y.)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1097/pp9.0000000000000026\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Progress in preventive medicine (New York, N.Y.)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1097/pp9.0000000000000026","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Introduction: Sodium, an important dietary requirement, is essential to many physiologic processes. High sodium intake affects serious health issues such as hypertension and cardiovascular disease, the largest cause of death globally. Consequently, many health organizations have recommended substantial reductions in sodium intake, to as little as 1,500 mg/d. Yet limited understanding exists for the entire range of the effect of sodium between high intake and the recommendations. Methods: We built a simulation using equations from the Uttamsingh model of the renal system to simulate the long-term mean arterial pressure (MAP) across sodium intake ranges. We used another existing physiology simulation platform, HumMod-3.0.4, for comparison. We compared the simulation results with empirical studies done on the global population. Results: We find a linear increase in MAP for consumption above 4,000 mg/d, but nearly constant MAP between 1,200 and 4,000 mg/d. Below 1,200 mg/d, the system cannot maintain homeostasis. Conclusion: Supporting the U-shape theory of sodium intake, which posits that too-high and too-low sodium intake rates increase cardiovascular disease risks, our results suggest that the homeostatic regulation by antidiuretic hormone and aldosterone transitions from sodium retention to sodium excretion at around 4,000 mg/d (a value that varies across individuals and conditions), indicating sodium saturation and evolutionary optimality. Our findings are consistent with recent empirical studies on large populations globally. We suggest that the current low-level recommendations are not supported by this physiologic model analysis and would require more compelling evidence.