Researchers analyzed four international prospective studies and demonstrated that the association between sodium intake and cardiovascular disease or mortality is dependent on an individual’s hypertension status.


Since cardiovascular disease is the leading cause of death globally, it is not surprising that public health agencies aim to educate the public by addressing behavioural factors that may increase their risk of disease.  Sodium reduction, for example, has been heavily promoted since it is known that high sodium intake results in major health concerns.

However, it may not be appropriate for public health policies to recommend sodium reduction for the entire population. As reported in The Lancet, researchers have observed that high sodium intake is associated with increased risk of cardiovascular disease only in individuals with high blood pressure or hypertension. This was demonstrated through a systematic review of four large-scale prospective studies, where levels of sodium excretion through urine (as a measure of intake) and the risk of cardiovascular disease outcome events were determined in 133, 118 individuals (63, 559 with hypertension, 69, 559 without hypertension) from 49 countries.

Sodium, typically in the form of salt, is a positively charged ion required for normal bodily functions. For instance, it is important for generating electrical activity in our muscles and nerves for contraction and signal processing, respectively. Sodium also helps maintain fluid balance in the body, as it plays an active role in water retention during filtration by the kidneys. The body tightly regulates sodium levels through many interconnected processes in order to maintain an optimal range for physiological function. Nowadays, salt in the diet can be attained from a wide variety of processed foods as they become increasingly more accessible and affordable. Salt is also frequently added when cooking to enhance the taste and flavour of food. With more people shifting to high-salt diets, and away from a well-balanced diet, soaring rates of cardiovascular disease have been noted.

It has been previously reported that the association between sodium intake and cardiovascular disease or mortality adopts a U-shape, implying that the risk increases significantly at both high and low levels of consumption. To test whether hypertension has an effect on this relationship, researchers collected morning fasting urine samples from every participant and used the Kawasaki formula to estimate sodium excretion as a surrogate form of measurement for sodium intake. Recordings of blood pressure were obtained with an Omron automatic digital monitor. Individuals were deemed hypertensive if they had a blood pressure of 140/90 mmHg or if they were prescribed drugs for it beforehand. Standardised case-report forms were used during follow-up to gather information about any subsequent incidence of cardiovascular disease and mortality. Through statistical analysis, the relationship between estimated sodium excretion and risk of primary outcome (a composite of death, myocardial infarction, stroke, and heart failure) was obtained. Interaction tests were performed to observe whether associations were modified depending on hypertension status.

The findings have confirmed that the association between sodium intake and risk of cardiovascular disease does change depending on blood pressure levels. Individuals with hypertension were generally men, weighed more, were physically inactive, and had a previous history of cardiovascular disease and diabetes. It was shown that in comparison to a moderate level of sodium intake (4-5 g/day), consumption of either high levels (≥7g/day) or low levels (< 3g/day) were associated with an increased risk of primary outcome events among hypertensive individuals. This was consistent with previous prospective cohort studies. But for those without hypertension, sodium intake of ≥7g/day did not correlate to a higher risk of composite outcome, although intake of < 3g/day did. In other words, sodium intake is more strongly associated with higher blood pressure in individuals with hypertension, which represented only about 10% of participants in the study. Hence, the harmful effects of high sodium intake appear to be limited to these individuals only.

It is possible that the effect of sodium intake on cardiovascular outcomes is only partially modified through its effects on systolic blood pressure. Previous studies have reported that concentrations of renin, aldosterone, and catecholamines increase with low sodium intake, and that they were also associated with increased cardiovascular disease and mortality. In addition, other non-blood pressure mechanisms may be at play; therefore, further investigations are required to clarify the processes that affect the clinical outcomes observed. Researchers suggested that large-scale and long-term randomized controlled trials (RCT) are ideal for assessing the effects, which would then be able to guide and reform public policies.




Written By: Michelle Tu, BSc

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