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Hypertension, stroke and salt sensitivity in East Asians

Hypertension, stroke and salt sensitivity in East Asians

Salt sensitivity of blood pressure (BP) is usually defined as a substantial change in BP parallel to changes in sodium intake, such as a difference in systolic BP ≥10 mmHg between high and low sodium intake protocols. It is generally thought that Asians and African–Americans are more likely to have higher salt sensitivity than people of European origin.1 Salt intake is also higher in some Asian countries than in many Western populations.2 The increased frequency of salt sensitivity in Japanese compared with Caucasians was reported to be partly related to increased frequencies of variants in candidate genes, such as those related to the renin-angiotensin system (RAS).3 This probably also applies to other East Asian populations.

Animal models of salt sensitivity with inbred rats show the condition can be genetically determined but in hypertensive patients there is no simple genetic test to diagnose salt sensitivity and it is usually considered to have a polygenic background. It seems likely that in the future, a genetic risk score comprising multiple single nucleotide polymorphisms may be useful to identify subjects who are salt-sensitive (SS) or salt-resistant (SR), which may have an impact on the choice of pharmacotherapy or advice about salt intake. The protocols to identify salt sensitivity are quite demanding and are not usually performed in everyday clinical practice and sodium intake or excretion are not commonly measured, so most hypertensive patients are not defined as SS or SR. Measurement of plasma renin might help to characterize sodium status, but this is not routine in all hypertension clinics.

The pathophysiology of salt sensitivity has also been debated. The classical understanding is that SS subjects require a hypertensive response to maintain normal plasma volume.1 An alternative theory is that differences in water balance between SS and SR subjects indicate differences in salt and water storage in the interstitial compartment that may relate to vascular dysfunction in those who are SS.4

The report of the Salt Reduction Committee of the Japanese Society of Hypertension concluded that salt restriction reduced the risk of cardiovascular diseases and may decrease the risk of stroke more than that of ischaemic heart disease.5 They also noted that excess salt intake increased the risk of left ventricular hypertrophy, heart failure, the urinary protein/albumin levels and end-stage renal failure in small-scale studies. In population studies, such as the INTERMAP (International Study on Macro/Micronutrients and Blood Pressure), dietary salt intake is usually directly related to BP but the relationship may be attenuated with control for body mass index.6

The 2018 report from the large-scale epidemiological cohort PURE (Prospective Urban Rural Epidemiology) study found that mean systolic BP increased by 2·86 mm Hg per 1 g increase in mean estimated sodium intake, but the associations between sodium intake and systolic BP were only positive in the communities in the highest tertile of sodium intake.7 The estimate of 24 hour sodium and potassium excretion as a surrogate for intake was based on morning fasting urine samples, which may not always be accurate. There was a significant inverse association between mean sodium intake and major cardiovascular events in the lowest tertile of sodium intake and a positive but non-significant association in the highest tertile, which was primarily due to stroke. There was a strong association of mean sodium intake with stroke in China where the mean intake was 5·58 g/day, but this was not seen in other countries where the mean intake was <5·0 g/day. A surprising finding was inverse relationships for sodium intake with myocardial infarction and total mortality, which were only significant after multivariable adjustment. However, all major cardiovascular outcomes decreased with increasing potassium intake in all countries.

This study has provided some food for thought, and for debate.8 It seems prudent to reduce sodium intake for those taking more than 5 g per day, but whether lower targets are appropriate may have to be reconsidered. There has been concern that excessive salt restriction might increase other cardiovascular risk factors, which could increase the risk for ischaemic heart disease.

A study in Chinese postmenopausal women (mean age 57.7 years) with prehypertension in Hong Kong found the mean (SD) urine sodium excretion was 133.9 (55.5) mmol per day, equivalent to a salt intake of 7.8 (3.2) g per day.9 The main food sources of salt were soup, rice and noodles, baked cereals, salted/preserved foods, Chinese dim sum and seafoods and intake of additional discretionary salt was relatively low. Other studies have shown a more substantial contribution from discretionary salt in condiments such as soy sauce and that might be more amenable to change.

Considering that salt sensitivity is not routinely assessed in individual patients with hypertension or prehypertension it may be better to adopt a general population approach that is more intensive in those at risk for high BP and related outcomes. Salt restriction may be more relevant in East Asian populations where the salt intake is high and stroke is more prevalent than ischaemic heart disease. As for potassium, the major dietary sources are from fruit and vegetables, so the simple bottom-line advice may be to reduce the discretionary use of salt for those with a high salt intake and to increase the intake of fruit and vegetables for everyone.


References

  1. Elijovich F, Weinberger MH, Anderson CA, et al. Salt sensitivity of blood pressure: A scientific statement from the American Heart Association. Hypertension 2016;68:e7-e46.
  2. Kario K, Chen CH, Park S, et al. Consensus document on improving hypertension management in Asian patients, taking into account Asian characteristics. Hypertension 2018;71:375-82.
  3. Katsuya T, Ishikawa K, Sugimoto K, et al. Salt sensitivity of Japanese from the viewpoint of gene polymorphism. Hypertens Res 2003;26:521-5.
  4. Laffer CL, Scott RC 3rd, Titze JM, et al. Hemodynamics and salt-and-water balance link sodium storage and vascular dysfunction in salt-sensitive subjects. Hypertension 2016;68:195-203.
  5. Ando K, Kawarazaki H, Miura K, et al. [Scientific statement] Report of the Salt Reduction Committee of the Japanese Society of Hypertension (1) Role of salt in hypertension and cardiovascular diseases. Hypertens Res 2013;36:1009-19.
  6. Stamler J, Chan Q, Daviglus ML, et al. Relation of dietary sodium (salt) to blood pressure and its possible modulation by other dietary factors: The INTERMAP study. Hypertension 2018;71:631-7.
  7. Mente A, O'Donnell M, Rangarajan S, et al. Urinary sodium excretion, blood pressure, cardiovascular disease, and mortality: a community-level prospective epidemiological cohort study. Lancet 2018;392:496-506.
  8. Messerli FH, Hofstetter L, Bangalore S. Salt and heart disease: a second round of "bad science"? Lancet 2018;392:456-8.
  9. Liu ZM, Ho SC, Tang N, et al. Urinary sodium excretion and dietary sources of sodium intake in Chinese postmenopausal women with prehypertension. PLoS One 2014;9:e104018.

Brian Tomlinson

Specialist in Internal Medicine & Clinical Pharmacology
Department of Medicine and Therapeutics
Adjunct Professor
The Chinese University of Hong Kong
Hong Kong, China
Hypertension
salt sensitivity
Stroke
sodium
potassium