Key result
Simulation models show sodium intake above 4,000 mg/d linearly increases MAP, with constant pressure below.
Why the study?
Limited understanding exists regarding the entire range of sodium effects between high intake levels and low-level recommendations of 1,500 mg/d.
Does varying sodium intake affect long-term mean arterial pressure in physiological simulation models?
Does varying sodium intake affect long-term mean arterial pressure in physiological simulation models?
Physiological simulation models suggest that sodium intake between 1,200 and 4,000 mg/d maintains constant mean arterial pressure, challenging current low-level sodium recommendations.
Challenges low-sodium targets in models; leaves open clinical validation before guideline changes.
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.
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Shen et al. (2019) studied Sodium intake and mean arterial pressure. Sodium intake was evaluated on Long-term mean arterial pressure (MAP). Physiologic simulation models showed a linear increase in mean arterial pressure for sodium consumption above 4,000 mg/d, but nearly constant pressure between 1,200 and 4,000 mg/d.
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