![](http://gpvoice.com.au/wp-content/uploads/2024/07/chef_salt_pepper_800_clr_5286.png)
High salt intake is said to independently contribute to high blood pressure and ultimately, increase cardiovascular disease (CVD). There are also many other diseases that are similarly associated with high salt intake. How robust is the evidence though? As we ponder about the associations, we may or may not push the message of salt reduction as strongly as we should. What about patients who are normotensive? Do they benefit from salt reduction as well? How much is high salt intake anyway?
What is low salt? What is low sodium?
The term sodium and salt are used interchangeably. 2.5g of salt contain 1g of sodium. When we talk about “salt” we often refer to sodium chloride (NaCl) although we also have potassium salt (KCl). For several million years, the main source of salt for human ancestors was that naturally found in foods, and salt intake then was below 0.5 g/day (1). People used to mine or produce salt through the evaporation of salt water. Historically, salt was also a valuable commodity which was bought and sold for thousands of years. It was also used by governments as a means of taxation.
Salt was used primarily as a preservative back then. Although refrigeration technologies obviate the need for salt as a preservative, the current salt intake averages >10 g/day in most countries, representing a >20 times increase in a short period of time in the evolutionary timescale. 10g of salt a day may not seem a lot but a 70kg body contains about 70g of sodium. So, an intake of >10g of salt a day is actually massive.
In high income countries (HICs), 80% of the salt in the diet is from processed, restaurant, and fast foods. In low- and middle-income countries (LMICs), most of the salt comes from that added by the consumer during cooking or in sauces.
The rationale behind why low salt should benefit
There are multiple mechanisms that relate increase salt intake to BP but there are probably many other mechanisms yet to be elucidated. Increased sodium intake leads to an increase in extracellular volume because of increased thirst and increased water retention. Excess salt intake would normally reduce sodium reabsorption because salt suppresses the renin-angiotensin-aldosterone system (RAAS) but if renal function is impaired, then the RAAS is impaired. A small increase in salt intake induces a greater rise in BP.
Changes in plasma sodium can also directly affect BP independent of the increase in extracellular volume. Changes in plasma sodium affects:
- The brain including cerebral infarct and haemorrhage, white matter lesions, cognitive impairment
- The heart and its vasculature including myocardial fibrosis, left ventricular dysfunction, LVH
- Inflammatory mechanisms including endothelial damage and oxidative stresses
- Kidney damage including renal fibrosis, haemodynamic changes, glomerular damage, proteinuria
- The immune system including proinflammatory pathways
- Gut microbiome damage (1)
The Evidence
Salt intake and BP
Way back in 1988, International Study of Sodium, Potassium, and Blood Pressure (INTERSALT), explored the relationship between 24 hour urinary electrolyte excretion and blood pressure (2). 10,079 men and women aged 20-59 were sampled from 52 centres around the world. Sodium excretion ranged from 0-2 mmol/24 hr amongst the Yanomamo Indians, Brazil to 242 mmol/24 h in North China. It demonstrated a direct association between salt intake as measured by 24-h urinary sodium and BP. This finding was confirmed by multiple other large epidemiological studies (3,4) and natural experiments at population level (5,6). It also found that salt reduction slowed down the rise in BP with aging.
Salt reduction and BP reduction
Another way to explore the association between salt and BP is to reduce salt intake and see what it does to the BP. There have been a large number of meta-analyses of randomised salt reduction trials over the years (see Figure 1). Pretty much all of them showed statistically significant reduction in BP although the degree of reduction varied because of the different inclusion criteria and different populations. Not unexpectedly, the falls in BP are larger in individuals who are hypertensive, black, and older compared with individuals who are normotensive, white, and young, respectively. This is likely related to the degree of RAAS response in those different populations.
Now, sometimes acute and large reductions in salt intake may trigger compensatory response in RAAS and sympathetic system which may lead to short term relative increase in plasma lipids. Perhaps, this may be the reason why Graudal et al challenged the salt reduction dogma in a Cochrane Systematic review in 2017 (7).
A dose-response relationship between salt intake and BP has also been demonstrated (8-10) perhaps most compellingly by 2 well-controlled trials where participants were assigned different levels of salt intake: 11.2, 6.4, and 2.9 g/day in one (9); and 8, 6, 4 g/day in the other (10). Both trials demonstrated that BP changes with salt intake, so that the lower the salt intake, the lower the BP.
The World Health Organization recommended that intake of 5 g/day will bring health gains. The U.K. National Institute for Health and Care Excellence has recommended 3 g/day as the long-term population salt intake target. In the United States, 4 g/day has been recommended for >50% of the population including blacks, individuals >50 years old, and those with hypertension, diabetes, or chronic kidney disease.
Salt and CVD
Reducing salt intake appears to reduce vascular events – ischaemic heart disease, heart failure, hypertensive heart disease and strokes. This is independent of reduction in BP. Most but not all studies or meta-analysis show a linear relationship between salt intake and CVD. However, Mente et al. have stirred controversy and confusion, as the investigators reported J or U-shaped associations, that is, both low and high salt intakes being associated with an increased risk (11,12). It is argued that association seen between a lower salt intake and higher CVD risk is explained by these individuals’ underlying diseases rather than their salt intake.
There was further debate on how salt intake is measured. When measured with multiple non-consecutive 24-h urinary sodium excretions, the relationship between salt intake and CVD events and all-cause mortality was direct and linear, down to a level of 3 g/day. However, when estimating salt intake by applying the formulas developed for spot urine samples on sodium concentrations, the relationship appeared J- or U-shaped.
Salt and other diseases
High salt intake is also associated with many other health conditions including kidney disease, renal stones, osteoporosis, stomach cancer, and obesity. For example, modest reductions in salt intake significantly reduced 24-h urinary albumin and protein excretion in individuals with hypertension, diabetes, and CKD. Lower salt intake could slow down CKD progression.
Increased salt intake and its effects on other organ systems:
- Stomach cancer has been linked to salt intake; Salt intake is closely associated with the risk of helicobacter pylori infection
- Risk of renal stones – increasing urinary calcium excretion.
- Loss of hip bone density in postmenopausal women
- Increased risk of overweight and/or obesity, independent of total calorie or sugar-sweetened beverage consumption
- Animals and humans studies have suggested a link with cognitive impairment and Alzheimer disease
Is salt reduction cost effective?
In HIC, population-wide salt reduction is highly cost effective and cost-saving in reducing CVD and premature deaths. It is estimated that the United Kingdom’s salt-reduction program has prevented ~9,000 CVD deaths per year and saved the health care service ~£1.5 billion per annum. By getting all companies to work toward the same targets, the United Kingdom has achieved a 20% to 50% reduction in the salt content of many food products over a decade, leading to concurrent falls in population salt intake, BP, and CVD mortality (9). Australia, Canada and USA have followed the UK model of voluntary targets.
Another way of achieving the results is to replace regular salt with salt substitutes, which are made with less sodium and more potassium and have been shown to reduce BP and CVD mortality.
In summary, the evidence surrounding the association between salt and BP is solid. The association is further bolstered by evidence linking salt reduction and benefits in not just BP lowering but also in other organ systems. We should all speak the same language when we advise our patients on the benefits of salt reduction while efforts with industry is in progress. For those who is not able to reduce “salt” intake, perhaps, replacement with potassium salt could be an option. Remember, the largest intake of salt in Western diets is through processed foods, so it is not just about stopping the sprinkling of salt on the food. It is about reading labels and choosing low salt foods.
Do you have time for a 5 min survey?
Please share your thoughts through a 5-10 minute survey found here:
https://unsw.au1.qualtrics.com/jfe/form/SV_dg7
This research study has been approved by The University of New South Wales Human Research Ethics Committee (iRECS6365).
References:
- He FJ, Tan M, Ma Y, MacGregor GA. Salt Reduction to Prevent Hypertension and Cardiovascular Disease: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020 Feb 18;75(6):632-647
- Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion. Intersalt Cooperative Research Group. BMJ. 1988 Jul 30;297(6644):319-28. doi: 10.1136/bmj.297.6644.319
- Zhou BF, Stamler J, Dennis B, et al., for the INTERMAP Research Group. Nutrient intakes of middle-aged men and women in China, Japan, United Kingdom, and United States in the late 1990s: the INTERMAP study. J Hum Hypertens 2003;17:623–30.
- Khaw KT, Bingham S, Welch A, et al. Blood pressure and urinary sodium in men and women: the Norfolk Cohort of the European Prospective Investigation into Cancer (EPIC-Norfolk). Am J Clin Nutr 2004;80:1397–403.
- He FJ, Pombo-Rodrigues S, MacGregor GA. Salt reduction in England from 2003 to 2011: its relationship to blood pressure, stroke and ischaemic heart disease mortality. BMJ Open 2014;4: e004549.
- Karppanen H, Mervaala E. Sodium intake and hypertension. Prog Cardiovasc Dis 2006;49:59–75.
- Graudal NA, Hubeck-Graudal T, Jurgens G. Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride. Cochrane Database Syst Rev 2017;4:CD004022.
- He FJ, MacGregor GA. How far should salt intake be reduced? Hypertension 2003;42: 1093–9.
- MacGregor GA, Markandu ND, Sagnella GA, Singer DR, Cappuccio FP. Double-blind study of three sodium intakes and long-term effects of sodium restriction in essential hypertension. Lancet 1989;334:1244–7.
- Sacks FM, Svetkey LP, Vollmer WM, et al., for the DASH-Sodium Collaborative Research Group. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. N Engl J Med 2001;344:3–10.
- 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.
- Mente A, O’Donnell M, Rangarajan S, et al., for the PURE, EPIDREAM, and ONTARGET/TRANSCEND Investigators. Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies. Lancet 2016;388:465–75.