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The Harm of Table Salt Is Exaggerated


  • The Harm of Table Salt Is Exaggerated

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    Reducing sodium intake with table salt lowers blood pressure in people with high blood pressure. Therefore, public health authorities recommend a low dietary sodium intake (<2.3 g / day) to lower blood pressure, which is equivalent to less than 5.7 g / day of salt (NaCl).

    This is expected to reduce cardiovascular outcomes (stroke, heart attack, etc.).

    However, a research team from Australia demonstrated that lower sodium intake is paradoxically associated with higher cardiovascular and all-cause mortality in people with diabetes.

    The physiological nature of these observations was not fully understood. Thus, in people without diabetes, low sodium intake may be associated with endothelial dysfunction.

    These pleiotropic effects may negate the benefits of low sodium blood pressure lowering since endothelial dysfunction independently contributes to cardiovascular disease associated with morbidity and mortality.

    A new randomized controlled trial tested the effects of salt supplementation in people with type 2 diabetes who routinely consume less than 3.5 grams of sodium (8.6 grams of salt) per day.

    Since low sodium intake may be associated with activation of the sympathetic nervous system and endothelial dysfunction (endothelial dysfunction is seen as a cause of vascular atherosclerosis), Australian researchers hypothesized that salt supplementation would decrease sympathetic nervous system activity and improve vascular endothelial function compared with placebo ( placebo - a pacifier disguised as a salt capsule).

    Why was the 3.5 g sodium per day selected for patient selection? This is because this level was associated with higher all-cause mortality in early observational studies for people with type 2 diabetes.

    Besides, public health authorities advocate a low sodium intake of 2.3 g / day.

    The study involved 22 patients aged 50-75 years, with a body mass index of 25-35 m2, with systolic blood pressure lower than 140 mmHg, and with diastolic - lower than 80 mm mmHg.

    For participants with high blood pressure, to correctly assess the degree of activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system, drugs affecting these systems were temporarily replaced with others.

    The participants were given capsule supplements of salt (NaCl 5.8 g / day) or placebo. Saline supplements (NaCl 5.8 g / day) or corresponding placebo capsules were taken daily for three weeks.

    All participants were divided into salt-resistant and non-salt resistant. In this study, salt tolerance was defined as an increase in mean 24-hour blood pressure of at least 4 mmHg when adding a capsule with salt.

    Arterial stiffness did not change in patients NOT RESISTANT to salt compared with placebo. Blood pressure increased by 4 mmHg. The activity of the sympathetic nervous system increased significantly after the addition of salt. But the indicators of endothelial function did not change.

    In patients RESISTANT to salt compared with the placebo group, blood pressure decreased by 3.8 mmHg. Sympathetic nervous system activity increased to a lesser extent after salt addition than in salt-sensitive patients.

    The overall activity of the sympathetic nervous system was significantly higher after salt addition in salt-sensitive individuals as compared to salt-sensitive individuals. However, after salt addition, endothelial function scores tended to be improved in salt-resistant patients.

    Salt supplementation increased sympathetic activity, but no signs of endothelial dysfunction. Also, cardiac baroreflex function improved and the activity of the renin-angiotensin-aldosterone system, as measured by serum aldosterone, was decreased.

    Salt-tolerant individuals have shown a trend towards improved endothelial function after salt supplementation.

    These results suggest that the role of severe sodium reduction in people with type 2 diabetes, especially those who are salt-tolerant, may be over-played

    In people with essential hypertension (high blood pressure), high salt intake increases blood pressure.

    However, in young healthy people (without hypertension), even a high salt intake for 9-10 days does not increase blood pressure levels, which was shown in a controlled study in which 3 groups of people consumed different amounts of salt: 2.6 grams/day, 6 g / day and 18 g / day, respectively.

    Although the long-term effects of increased salt intake may be different, high salt intake is associated with increased mortality.

    Salt or Sugar?

    But it is not yet clear whether this is due to high salt intake or whether the rise in blood pressure is due to a higher intake of sugary drinks to quench the thirst caused by overly salty foods.

    So, in recent years, more and more data have been accumulating that the risk of developing hypertension and cardiometabolic disorders is more associated with increased consumption of sugars, and not salt (as previously thought).

    The harm of salt is probably exaggerated, although it cannot be completely ignored.

    The mechanisms by which high sugar intake raises blood pressure may be by stimulating the activity of the sympathetic nervous system, increasing the secretion of the hormone renin, sodium retention in the kidneys, increasing leptin levels, and decreasing nitric oxide, which results in high blood pressure.

    Both excess salt and salt deficiency are associated with a higher risk of mortality.

    Both excess salt and salt deficiency can promote the activation of the renin-angiotensin-aldosterone system (the system that regulates blood pressure), which ultimately leads to high blood pressure, as shown in an experiment in rats by researchers at the Department of Pharmaceutical Pharmacology, Ruprecht-Karls University Heidelberg, Germany.

    That is, the amount of salt in the body must be optimal. Excessive salt intake, as well as salt deficiency, have been associated with higher mortality risk in people with type 1 diabetes.

    And too low salt intake (0.03% sodium in the diet) for 6 weeks in transgenic mice prone to atherosclerosis, despite slightly lower blood pressure, led to a 4-fold increase in the accumulation of cholesterol plaques in comparison with the same mice eating more salt (0.3% sodium in the diet).

    This was associated with the activation of the renin-angiotensin-aldosterone system, increased vascular expression of adhesion molecules, and inflammatory cytokines.

    Why does the body react to a complete rejection of salt by increasing blood pressure?

    Probably because the first animals lived in the sea.

    The marine habitat is rich in salt. Salt retains fluid in the body and maintains normal homeostasis. Over time, the animals came out onto land. But there is little salt on land.

    And the role of the pressure regulator was taken over by the Renin Angiotensin Aldosterone Hormonal System (RAAS), as well as the sympathetic nervous system.

    When there is a salt deficiency in the body, the RAAS begins to activate to prevent a loss of pressure that is critical for life, and pressure rises again.

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