Sodium Intake and Target Organ Damage in Hypertension—An Update about the Role of a Real Villain

Federica Nista, Federico Gatto, Manuela Albertelli and Natale Musso
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Federica Nista: Unit of Hypertension, Clinical Endocrinology, Department of Internal Medicine, Ospedale Policlinico San Martino Genova, University of Genoa Medical School, 6-16132 Genoa, Italy
Federico Gatto: Unit of Hypertension, Clinical Endocrinology, Department of Internal Medicine, Ospedale Policlinico San Martino Genova, University of Genoa Medical School, 6-16132 Genoa, Italy
Manuela Albertelli: Unit of Hypertension, Clinical Endocrinology, Department of Internal Medicine, Ospedale Policlinico San Martino Genova, University of Genoa Medical School, 6-16132 Genoa, Italy
Natale Musso: Unit of Hypertension, Clinical Endocrinology, Department of Internal Medicine, Ospedale Policlinico San Martino Genova, University of Genoa Medical School, 6-16132 Genoa, Italy

IJERPH, 2020, vol. 17, issue 8, 1-13

Abstract: Salt intake is too high for safety nowadays. The main active ion in salt is sodium. The vast majority of scientific evidence points out the importance of sodium restriction for decreasing cardiovascular risk. International Guidelines recommend a large reduction in sodium consumption to help reduce blood pressure, organ damage, and cardiovascular risk. Regulatory authorities across the globe suggest a general restriction of sodium intake to prevent cardiovascular diseases. In spite of this seemingly unanimous consensus, some researchers claim to have evidence of the unhealthy effects of a reduction of sodium intake, and have data to support their claims. Evidence is against dissenting scientists, because prospective, observational, and basic research studies indicate that sodium is the real villain: actual sodium consumption around the globe is far higher than the safe range. Sodium intake is directly related to increased blood pressure, and independently to the enlargement of cardiac mass, with a possible independent role in inducing left ventricular hypertrophy. This may represent the basis of myocardial ischemia, congestive heart failure, and cardiac mortality. Although debated, a high sodium intake may induce initial renal damage and progression in both hypertensive and normotensive subjects. Conversely, there is general agreement about the adverse role of sodium in cerebrovascular disease. These factors point to the possible main role of sodium intake in target organ damage and cardiovascular events including mortality. This review will endeavor to outline the existing evidence.

Keywords: sodium intake; organ damage; hypertension; cardiovascular risk (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2020
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