Dietary Sodium Reduction Lowered Blood Pressure in Most Middle-Aged to Elderly Adults, Independent of Hypertension Status
Authors:
Evan Bloch
BA Candidate, Department of Neuroscience, Dartmouth College
Michael Bloch, MD, FACP, FASH, FNLA, FAHA, FSVM
Associate Professor, University of Nevada/Reno School of Medicine
Medical Director, Vascular Care, Renown Institute for Heart and Vascular Health
Sodium is a dietary component known to substantially contribute to blood pressure (BP), and the estimated daily average sodium intake among middle-aged to elderly adults in the United States exceeds most dietary recommendations. Earlier studies indicate that approximately 25% to 50% of individuals exhibit BP variation in response to sodium intake—known as salt sensitivity of BP (SSBP)—however, these studies are limited and may underestimate the impact of dietary salt reduction on BP.1 Moreover, previous studies tend to exclude participants who are normotensive and participants who are taking antihypertensive medications.1
The Coronary Artery Risk Development in Young Adults (CARDIA)-SSBP was designed to investigate the within-individual BP response to dietary sodium increase and decrease across a wide spectrum of individuals from normotensive through treated and untreated hypertension. Enrollment for the prospective, multicenter, observational cohort study occurred through two sources from April 2021 through February 2023. Initially, enrollment in 2021 only included patients from CARDIA (an ongoing longitudinal study beginning in 1985 that aimed to identify factors in young adulthood that may contribute to the development of cardiovascular disease). There was an amendment in 2022 to include non-CARDIA participants from Chicago and Birmingham sites.2 Patients who were eligible for the trial were aged 50 to 75 years, with key exclusion criteria of enrollment visit systolic BP outside 90 to 160 mmHg, diastolic BP outside 50 to 100 mmHg, with contraindications to high- or low-sodium diets, or resistant hypertension.
Eligible patients were initially randomly allocated to either a high- or low-sodium diet for one week. After 1 week, each patient crossed over to the other diet; thus, each patient served as their own control. The high-sodium diet was achieved by daily supplementation of 2 bullion packets, each containing 1100 mg of sodium to each participant’s usual diet. The low-sodium diet was designed to provide 500 mg/d of sodium, approximately 4500 mg/d of potassium, and approximately 1000 mg/d of calcium. The food was prepared in metabolic kitchens that were standardized across sites. Patients on the low-sodium diet were asked not to consume any food that was not prepared from the metabolic kitchen. Each patient attended four study visits: (1) enrollment; (2) baseline; (3) end of the first diet week; (4) and end of the second diet week. For an assessment of dietary adherence, 24-hour urinary sodium and 24-hour ambulatory BP were obtained at baseline and after each weekly diet.
Among the total of 213 eligible patients who completed the study, 25% were normotensive, 20% had controlled hypertension, 31% had treated but uncontrolled hypertension, and 25% had untreated hypertension. The median age was 61 years, 65% were female, and 64% were Black. The mean baseline ambulatory BP was 127 to 128/77-80 mmHg. Using the 24-hour urine excretion assessment, it was determined that the baseline diet had a median urine excretion of 4.45 g/d, while the high- and low-salt diet effectively raised and lowered the medians to 5.00 g/d and 1.27 g/d, respectively.
The median within the individual change in 24-hour mean arterial ambulatory systolic BP from high- to low-sodium diet was 4 mm and showed no significant variation among the subgroups. A decrease in mean arterial pressure was demonstrated in 73.4% of participants, with the other 26.6% either showing no change or a slight increase in arterial pressure. Similarly, 71.7% of individuals showed a decline in systolic BP from baseline on the low-sodium diet, without showing a significant increase in systolic BP from baseline on the high-sodium diet. This reduction in BP in response to a lower sodium diet was consistent across subgroups, including age, sex, and race, with relatively greater effects in individuals with higher baseline BP and diabetes. Adverse events were reported in 9.9% and 8.0% of individuals while consuming high- and low-sodium diets, respectively, with the most commonly reported effects being gastrointestinal discomfort, headache, and edema on the high-sodium diet and cramping and weakness on the low-sodium diet.
These data confirm that a low-sodium diet is capable of lowering BP in individuals with normotension, controlled hypertension, untreated hypertension, and uncontrolled hypertension. The reductions demonstrated are similar to what would be expected with a single, low-dose anti-hypertensive medication, like hydrochlorothiazide 12.5 mg/d, or even renal denervation. Similar to drug and device studies, the magnitude of BP reduction seen here was greater in patients with higher baseline BP. If the study had been performed in patients with a higher baseline BP, the results would have likely been more substantial. The results of this study suggested that about 50% of patients were highly salt sensitive, but it is important to recall that there is some degree of variability in serial measurements of ambulatory BP, making it difficult to characterize individual patients.
CARDIA-SSBP showed that a low-sodium diet significantly reduces BP consistently across the spectrum from normotensive to hypertensive, treated and untreated, controlled and uncontrolled. The use of ambulatory BP monitoring as the primary endpoint and measurement of 24-hour urinary sodium to confirm dietary sodium are important strengths of the study. The limitations of this study, however, come from its applicability to clinical practice. The crossover study design was elegant, but even with the use of a metabolic kitchen supplying all meals for the low-salt diet, the mean dietary intake was nearly 1.2 g/d, which was far above the target of 0.5 g/d. Interventions work only as long as patients follow them. It seems unlikely that most patients would be able to maintain this degree of low-sodium diet over the long term without the use of a specialized metabolic kitchen. It seems clear that a low-salt diet would be helpful for our patients.
References:
1. Bailey MA, Dhaun N. Salt Sensitivity: causes, consequences, and recent advances. Hypertension. doi:10.1161/HYPERTENSIONAHA.123.17959
2. Gupta DK, Lewis CE, Varady KA, et al. Effect of dietary sodium on blood pressure: a crossover trial. JAMA. 202;330(23):2258-2266. doi:10.1001/jama.2023.23651