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High-Salt Diet May Boost Cortisol

<ѻý class="mpt-content-deck">— Eating a diet high in sodium increased levels of cortisol and other metabolites, potentially giving rise to metabolic syndrome, researchers found.
Last Updated May 21, 2013
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Eating a diet high in sodium increased levels of cortisol and other metabolites, potentially giving rise to metabolic syndrome, researchers found.

In a cross-sectional study, levels of sodium in the urine were significantly associated with both urinary free cortisol and cortisol metabolites (P<0.001 for both), Rene Baudrand, MD, of Pontificia Universidad Catolica de Chile in Santiago, and colleagues reported online in Clinical Endocrinology.

And patients who had high sodium intake had more insulin resistance as measured by an insulin resistance index (HOMA-IR, P=0.04) and more metabolic syndrome (P<0.001), they reported.

Action Points

  • Note that this cohort study demonstrated an association between high sodium intake and urinary cortisol levels.
  • Be aware that a mechanistic link between sodium intake and elevation in cortisol was not addressed.

A diet high in sodium has long been associated with hypertension, dyslipidemia, and other cardiovascular effects. The research team recruited 370 patients, ages 18 to 85, in order to determine if a high-salt diet can affect cortisol levels and, subsequently, the metabolic syndrome.

The mostly female (70%) cohort's mean body mass index (BMI) was 29.3 kg/m2, and 70% of patients had a diet that was high in sodium.

A little over 60% were categorized as having metabolic syndrome based on waist circumference, high-density lipoprotein (HDL) cholesterol levels, triglycerides, systolic blood pressure, and fasting glucose.

The researchers measured plasma hormones, urinary free cortisol, cortisol tetrahydrometabolites, and performed a lipid profile after participants sustained a 12-hour fasting period.

Overall, they found urinary sodium levels were positively correlated with urinary free cortisol and cortisol metabolites, as well as with glycemia (P=0.04) and anthropometric variables such as weight (P<0.001) and BMI (P=0.02).

Urinary sodium levels were inversely associated with levels of adiponectin (P=0.004), HDL cholesterol (P=0.007), and aldosterone (P=0.002).

Age, low-density lipoprotein (LDL) cholesterol, triglycerides, C-reactive protein, plasma cortisol, plasma cortisone, and leptin had no significant correlation with sodium intake, the researchers reported.

Adjusted models found that patients who had high sodium intake (>150 mEq/day) had higher levels of urinary free cortisol and cortisol metabolites (P<0.001 for both), increased insulin resistance as measured by HOMA-IR, and higher triglycerides (P=0.01) compared with patients who had normal sodium intake (50 to 149 mEq/day).

Those in the high-intake category also had lower adiponectin levels (P=0.01) and lower HDL cholesterol (P<0.05) than those with adequate intake, the researchers reported.

A linear regression model determined that increasing urinary sodium, as a continuous variable, was associated with an increasing number of variables of the metabolic syndrome (P<0.001).

A multivariate model adjusting for age, gender, and BMI showed a high discriminative capacity for metabolic syndrome, using four clinical variables -- high sodium intake, HOMA-IR, cortisol metabolism, and adiponectin -- although the latter had a protective effect.

"Our results suggest that a subtle increase in the overall glucocorticoid production may partially explain the metabolic disturbances observed with a liberal salt diet in addition to the well-documented risk of hypertension," the researchers wrote.

The study was limited by its observational nature, and that urinary free cortisol was not measured by gold standard (liquid chromatography-mass spectrometry) methodology, the researchers noted.

They added that the link between sodium intake and cortisol levels needs to be confirmed in future research. These studies should look into mechanisms by which increased salt intake may increase cortisol production and should assess whether other dietary factors, aside from sodium, may explain some of the effects seen in the study.

Disclosures

The study was supported by FONDEF, Fondecyt, and the Millennium Institute in Immunology and Immunotherapy.

The researchers reported no conflicts of interest.

Primary Source

Clinical Endocrinology

Baudrand R, et al "High sodium intake is associated with increased glucocorticoid production, insulin resistance, and metabolic syndrome" Clinical Endocrinol 2013; DOI: 10.1111/cen.12225.