Blood Pressure Increases Along with Sodium Intake

The association is most pronounced in hypertensives and consumers of high-sodium diets.
The association is most pronounced in hypertensives and consumers of high-sodium diets.

Increasing urinary sodium concentrations—a surrogate for sodium intake—are associated with increasing blood pressure, particularly among individuals consuming high-sodium diets, those with hypertension, and older people, according to a new report in The New England Journal of Medicine (2014;371:601-611).

In a study of 102,216 adults from 18 countries, researchers found that each 1-gram increment in estimated sodium excretion was associated with a 2.11 mm Hg increment in systolic blood pressure (SBP) and a 0.78 mm Hg increment in diastolic blood pressure (DBP). The association was most pronounced among subjects with a sodium excretion greater than 5 grams per day.

In these individuals, each 1-gram increment in sodium excretion was associated with a 2.58 mm Hg increment in SBP. Among those with a sodium excretion of 3–5 grams per day, each 1-gram increment in sodium excretion was associated with a significant 1.74 mm Hg increment in SBP. SBP increased by a non-significant 0.74 mm Hg per gram among those with a sodium excretion of less than 3 grams per day.

In addition, the researchers, led by Andrew Mente, PhD, of McMaster University in Hamilton, Ont., observed a more pronounced effect of sodium excretion on SBP among individuals with hypertension than those without hypertension. SBP increased by 2.49 mm Hg per gram of sodium excretion in hypertensives compared with 1.30 mm Hg per gram in non-hypertensives.

SBP increased by 2.97 mm Hg per gram among individuals aged 55 years and older, 2.43 mm Hg per gram among subjects aged 45–55 years, and 1.96 mm Hg per gram among those younger than 45 years.

Potassium excretion was inversely associated with SBP, significantly more so in individuals with hypertension than in those without it. Each 1-gram increment in potassium excretion per day was associated with a 0.75 mm Hg decrement in SBP and a 0.06 mm Hg decrement in DBP.

The investigators used fasting morning urine specimens to estimate 24-hour sodium and potassium excretion, and used these estimates as surrogates for sodium and potassium intake.

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