Nephrology Dialysis Transplantation

NDT Advance Access published online on May 2, 2008
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfn160

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Dietary sodium: the dark horse amongst cardiovascular and renal risk factors

Albert Mimran and Guilhem du Cailar

Department of Internal Medicine, Hôpital Lapeyronie, Montpellier Cedex, France

Correspondence and offprint requests to: Albert Mimran, Department of Internal Medicine, Hôpital Lapeyronie, 34295 Montpellier Cedex 5, France. Tel: +33-4-67-33-84-43; Fax +33-4-67-33-84-53; E-mail: amimran{at}wanadoo.fr

Keywords: left ventricular hypertrophy; microalbuminuria; sodium intake; hypertension

In American and European populations, the estimated median values of salt intake are 7 and 10 g/day in women and men, respectively. Whether these amounts of salt are inocuous or deleterious is a subject of large debate between pro [1–4] and con [5] recommendations of a large-scale reduction of sodium intake. In addition to the well-admitted effect of sodium on blood pressure, several clinical and experimental observations are in favour of non-pressure-related effects of salt that could contribute to its influence on cardiovascular outcome.

	Dietary salt and blood pressure

Top Dietary salt and blood... Non-pressure mediated effects of... Does the effect of... Is sodium reduction associated... Putative mechanism (s) involved... Conclusion References

 
In clinical research and practice, measurement of 24-h urinary sodium excretion is probably the most reliable estimate of sodium intake, with a variation coefficient of 20% [6]. Table salt accounts for 10%, whereas cooking and food salt represent 5 and 85% of total intake, respectively [7]. The use of the sodium-to-creatinine ratio on a single-spot urine sample, which is probably more convenient for population studies, may not be reliable, due to the strong infuence of age and gender on urinary creatinine.

In the Intersalt study [8] conducted in >10 000 male and female subjects aged 20–59 years, in 52 centres with mean values of 24-h natriuresis centre ranging from 0.5 mmol in Yanomamo Indians (Brazil) to 242 mmol/24 h in North China, a positive relationship between sodium intake and blood pressure or the prevalence of hypertension was found in 33/52 centres. Populations with a mean natriuresis of <55 mmol/24 h were characterized by lower blood pressure, low prevalence of hypertension (as low as 0.8% for a median natriuresis of 28 mmol/24 h in Papua New Guinea) and no increase in blood pressure with age. Of interest, the slope of the relationship between natriuresis and blood pressure tended to be steeper with increasing age, thus suggesting that sodium sensitivity may be more prevalent with older age [9]. Several studies of rather short duration have shown that reduction of salt intake is associated with a significant decrease in blood pressure. In the whole population of normotensive and hypertensive subjects maintained on their usual diet, the reduction of salt intake from 150 to 100 mmol/day (8.8–6 g/day sodium chloride), which is considered as acceptable, during a 4-week period was associated with a rather negligible decrease in blood pressure of 2.1/1.1 mmHg. Reducing sodium intake from 100 to 50 mmol/day (3 g/day sodium chloride) (considered as a drastic reduction in dietary sodium) resulted in an additional fall of blood pressure of 4.6/2.4 mmHg. In subjects constantly maintained on the DASH diet, the fall of blood pressure in response to the change from the high to the intermediate level of sodium intake was still negligible (–1.3/–0.6 mmHg). When the effect of the change from the high to intermediate sodium intake was considered, it was similar in normo and hypertensive people [10]. In a systematic review and meta-analysis of randomized controlled trials of various durations conducted in normotensive and untreated hypertensive populations, moderate reduction of sodium intake by an average of 40 mmol/24 h was associated with a fall in blood pressure of 8/4.3 mmHg in hypertensive subjects but no marked decrease in normal subjects (–2.3/–1.2 mmHg). No correlation between the degree of reduction of sodium intake and the change in blood pressure was detected. The authors concluded that ‘advice to reduce dietary sodium may help people on antihypertensive drugs to discontinue their medication while maintaining good blood pressure control’ [11].

	Non-pressure mediated effects of dietary sodium

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In essential hypertension, the presence of left ventriular hypertrophy (LVH) is a strong and independent predictor of increased cardiac and cerebrovascular [12] events and mortality; and in-treatment reduction in left ventricular mass (LVM) is associated with cardiovascular protection [13]. Recently, microalbuminuria (MA) (albuminuria between 30 and 300 mg/day) has emerged as a reliable predictor of cardiovascular risk in a large population [14], normotensive subjects [15] and essential hypertension [16], with a significant increase in risk >7 mg/day [17]. In addition, even for values well below the usually accepted threshold of 30 mg/day, albuminuria (UAE) predicted the subsequent development of hypertension in normotensive individuals [18].

The level of systemic pressure is the most powerful determinant of UAE and LVM, and several factors including overweight and C-reactive protein were shown to potentiate the relationship between arterial pressure and UAE [19].

Almost 20 years ago, Schmieder et al. [20] found a positive correlation between LVM index and sodium intake, estimated by 24-h natriuresis. The existence of this relationship, independent of blood pressure, was confirmed by us [21] and others [22]. In a totally ignored but interesting study conducted in 717 patients with essential hypertension and published in 1972, Swaye et al. [23] reported that, only in male subjects, the prevalence of electrocardiographic LVH was significantly higher in patients who added salt to food before tasting as compared to subjects who did not (39 versus 22%, P < 0.01). Natriuresis, which was measured in 47 individuals, averaged 151 mmol/day in salt-adders and 111 mmol/day in non-salt-adders. Of interest, the severity of hypertension was not influenced by salt intake in hypertensive men.

In a cohort of 336 normotensive (arterial pressure <140/90) subjects and 503 patients with never-treated essential hypertension, sodium intake was higher than 172 and 131 mmol/day (corresponding to 10 and 7.7 g sodium chloride) in 40% of men and women, respectively. A progressive increase in LVM index and UAE with increasing quintile of sodium intake was observed in the whole population, and the slope of the linear relationship between systolic arterial pressure and LVM index or UAE was progressively steeper from the lowest to the highest quintile of natriuresis [24]. In the normotensive cohort, multivariate analysis showed that echographic LVM index was positively correlated with natriuresis, independent of gender, age and mean arterial pressure, thus confirming our previous findings [21]. As shown in Figure 1, in 450 patients with never-treated hypertension, the prevalence of left ventricular hypertrophy (LVH), MA or both clearly increased from the lowest to the highest quintile of natriuresis, despite similar mean values of age and blood pressure in all quintiles of urinary sodium [24]. In contrast, in the cross-sectional study of the Framingham Offspring Study cohort conducted in 2660 individuals including 36% of participants with hypertension, no influence of sodium intake (estimated as the sodium-to-creatinine ratio on a single-morning-spot urine sample) on LVM was detected [25]. Nevertheless in the same population, a positive correlation between the sodium-to-creatinine ratio and albuminuria was recently reported [26]. Such a discrepancy may be related to the inaccuracy of the sodium-to-creatinine ratio, especially in elderly subjects, and the heterogeneity of the population.

View larger version (28K): [in this window] [in a new window] [Download PowerPoint slide]   Fig. 1 Prevalence of left ventricular hypertrophy (LVH 125 in men and 110 g/m2 in women), microalbuminuria (MA 20 µg/min in 24-h urine collection) or both (MA+ LVH+) according to quintiles of 24-h natriuresis in 450 patients with never-treated essential hypertension aged 40 years. Sodium intake was >100 mmol/24 h in subjects of quintile 3 in women and quintile 2 in men. Mean values of age and blood pressure were similar in all quintiles of urinary sodium excretion.

 
In our cohort, analysis of pulse pressure (PP), a marker of elastic artery stiffness and a predictor of cardiovascular events [27], showed that in subjects >40 years (>40 years of age PP is positively correlated with age, whereas it is negatively correlated with age <40 years), PP increased with increasing sodium intake [28]. The deleterious influence of sodium on the stiffness of large arteries, assessed by pulse wave velocity (PWV), was documented in a study showing a lower PWV in normotensive urban (Beijing area, mean natriuresis of 230 mmol/day) as compared to rural (Guangzhou area, natriuresis of 130 mmol/day) Chinese people [29]. In urban Australian volunteers, the same group demonstrated that a rather severe reduction of dietary salt to 44 mmol/day and for a period of 2 years resulted in a significant reduction in aortic PWV, independent of changes in blood pressure in normotensive individuals. Nevertheless, results should be taken with caution due to the notoriously poor reliability of dietary recall as well as the sodium-to-potassium ratio without determination of urinary creatinine as indexes of sodium intake [30].

	Does the effect of dietary sodium on the cardiovascular system translate into an influence on cardiovascular risk in observational studies?

Top Dietary salt and blood... Non-pressure mediated effects of... Does the effect of... Is sodium reduction associated... Putative mechanism (s) involved... Conclusion References

 
In 1998, analysis of the NHANES I (first National Health and Nutrition Examination Survey Epidemiologic Follow-up study) database concluded that sodium intake, as estimated by a single dietary recall, was inversely associated with cardiovascular and all-cause mortality [31]. In the NHANES II study reported in 2006, the same group confirmed their earlier findings, but no such association was detected for subjects aged <55 years, obese subjects and non-whites within a follow-up period of 13.7 years [32]. In a very recent longitudinal study conducted in 40 547 Japanese men and women aged 40–79 years and followed up for 7 years, Shimazu et al. [33] observed that the ‘Japanese dietary pattern’ (quite rich in salt) was associated with a decreased risk in cardiovascular mortality, as compared to ‘high-fruit and vegetable diet’. Only in overweight subjects, He et al. [34] reported that a 100 mmol increase in sodium intake (as estimated by dietary recall) was associated with an increase in stroke incidence of 32%, coronary heart disease mortality of 44% and overall cardiovascular mortality of 61%. In a Finnish population of 2436 individuals aged 25–74 years, with a remarkably high sodium intake (24-h natriuresis above 159 and 119 mmol/day in 75% of men and women, respectively), dietary sodium predicted mortality and risk of coronary heart disease, independent of blood pressure and other cardiovascular risk factors. These findings were restricted to obese men in whom for a 100 mmol increase in sodium intake, cardiovascular morbidity increased by 45%; however, no influence on acute stroke was detected [35]. The same group later reported that the risk of developing type 2 diabetes within a period of 18 years in 35- to 64-year-old Finnish people was markedly increased (RR 2.8) only in subjects of the fourth quartile (natriuresis >253 in men and >189 mmol/day in women) as compared to the lowest quartile associated [36].

	Is sodium reduction associated with reduction in cardiovascular risk in interventional studies?

Top Dietary salt and blood... Non-pressure mediated effects of... Does the effect of... Is sodium reduction associated... Putative mechanism (s) involved... Conclusion References

 
In the TONE study (Trial of Nonpharmacologic Interventions in the Elderly) [37] conducted in 681 treated hypertensive patients aged 60–80 years with blood pressure <145/85 mmHg while taking one medication, reduction of 24-h natriuresis to 80 mmol/day or less, alone or combined with body weight reduction, was proposed. After 3 months of dietary intervention, the medication was discontinued. Within a mean follow-up period of 27.8 months, the primary endpoint of blood pressure 150/90 mmHg or resumption of antihypertensive medication or a cardiovascular event occurred in 59% of subjects submitted to sodium reduction versus 73% in the group maintained on usual diet (HR of 0.68, P < 0.001). Resumption of antihypertensive treatment was necessary in 64% of the sodium-reduced versus 79% in the control group. However, no information on cardiovascular outcome was provided. The TOHP study (Trials for Hypertension Prevention) was conducted in subjects aged 30–54 years with ‘high-normal’ blood pressure. From baseline to 18 months, a net decrease in urinary sodium of 44 mmol/day (from a baseline value of 155 mmol/day) was associated with a significant change in blood pressure of –1.7/–0.8 mmHg, and a reduction by 26% of the incidence of denovo hypertension. In addition, the risk of a cardiovascular event was 25% lower in the sodium reduction intervention group after adjustment for age, gender and baseline natriuresis and body weight [38]. Nevertheless, there are some limitations of these studies, including post hoc analysis of two studies, no repeat assessment of compliance to dietary sodium restriction and finally the absence of any difference in mortality between low and normal salt intake.

Although in favour of a moderate reduction (by at least 30–40%) of dietary sodium, the results of the above-mentioned studies deserve to be confirmed.

	Putative mechanism (s) involved in the deleterious effect of salt

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Beyond an even minimal increase in systemic pressure and circulating or extracellular volume, several non-pressure-dependent consequences of increased sodium intake on widely accepted predictors of deleterious cardiovascular events, such as LVH and MA [24] as well as pulse pressure [28] and arterial stiffness [29], may explain an unfavourable effect of sodium on cardiovascular disease. The mechanisms of the prohypertrophic effects of dietary sodium on the cardiovascular system are still unclear. In rat studies, upregulation of type 1-angiotensin II receptors with prohypertrophic action [39] as well as downregulation of type 2-angiotensin II receptors with antihypertrophic properties [40], and an increase in the cardiac production of aldosterone, aldosterone synthase activity and CYP11B2 expression [41], together with the correction of salt-associated cardiovascular abnormalities by spironolactone [42] were demonstrated. Only in subjects with salt-sensitive hypertension, was it shown that plasma concentration of isoprostanes (as markers of superoxide generation) [43] or the endogenous inhibitor of nitric oxide synthesis (asymmetrical dimethyl arginine, ADMA) [44] were consistently increased after sodium loading; thus suggesting that high salt intake may exacerbate the generation of free radicals.

	Conclusion

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Until now, most debates have focused on the pressure effect of dietary sodium. Taking into consideration the presently reported findings on the non-pressure-related effects of salt on widely accepted markers of cardiovascular risk, such as left ventricular geometry, albuminuria or pulse pressure and the reduction by moderate and reasonable reduction of dietary sodium of the progression from pre- to sustained hypertension, it may be wise to favour a modest (30–40%) reduction in sodium intake to 5–7 g sodium chloride. Since no unpleasant effect of such a proposition has been reported, this could be achieved through education and ‘comprehensible labelling’ of processed foods (the main source of sodium).

Conflict of interest statement. None declared.

	References

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1. de Wardener HE, Kaplan NM. On the assertion that a moderate restriction of sodium intake may have adverse health effects. Am J Hypertens (1993) 6:810–814.[Web of Science][Medline]
2. Al-Awqati Q. Evidence-based politics of salt and blood pressure. Kidney Int (2006) 69:1707–1708.[CrossRef][Web of Science][Medline]
3. Cappuccio FP. Salt and cardiovascular disease. BMJ (2007) 334:859–860.[Free Full Text]
4. He FJ, de Wardener HE, MacGregor GA. Salt intake and cardiovascular mortality. Am J Med (2007) 120:55–59.
5. Alderman MH. Evidence relating dietary sodium to cardiovascular disease. J Am Coll Nutr (2006) 25(3 Suppl):256S–261S.[Abstract/Free Full Text]
6. Luft FC, Fineberg NS, Sloan RS. Estimating dietary sodium intake in individuals receiving a randomly fluctuating intake. Hypertension (1982) 4:805–808.[Abstract/Free Full Text]
7. Sanchez-Castillo CP, Warrender S, Whitehead TP, et al. An assessment of the sources of dietary salt in a British population. Clin Sci (Lond) (1987) 72:95–102.[Medline]
8. Intersalt Cooperative Research Group. Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion. BMJ (1988) 297:319–328.[Abstract/Free Full Text]
9. Law MR, Frost CD, Wald NJ. By how much does dietary salt reduction lower blood pressure? I—Analysis of observational data among populations. BMJ (1991) 302:811–815.[Abstract/Free Full Text]
10. Sacks FM, Svetkey LP, Vollmer. 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.[Abstract/Free Full Text]
11. Hooper L, Bartlett C, Smith GD, et al. Systematic review of long term effects of advice to reduce dietary salt in adults. BMJ (2002) 325:628–637.[Abstract/Free Full Text]
12. Verdecchia P, Porcellati C, Reboldi G, et al. Left ventricular hypertrophy as an independent predictor of acute cerebrovascular events in essential hypertension. Circulation (2001) 104:2039–2044.[Abstract/Free Full Text]
13. Devereux RB, Wachtell K, Gerdts E, et al. Dahlöf B. Prognostic significance of left ventricular mass change during treatment of hypertension. JAMA (2004) 17:2350–2356.
14. Hillege HL, Fidler V, Diercks GF. Prevention of Renal and Vascular End Stage Disease (PREVEND) Study Group. Urinary albumin excretion predicts cardiovascular and noncardiovascular mortality in general population. Circulation (2002) 106:1777–1782.[Abstract/Free Full Text]
15. Arnlöv J, Evans JC, Meigs JB, et al. Low-grade albuminuria and incidence of cardiovascular disease events in nonhypertensive and nondiabetic individuals: the framingham heart study. Circulation (2005) 112:969–975.[Abstract/Free Full Text]
16. Olsen MH, Wachtell K, Ibsen He. LIFE Study Investigators. Reductions in albuminuria and in electrocardiographic left ventricular hypertrophy independently improve prognosis in hypertension: the LIFE study. J Hypertens (2006) 24:775–781.[Web of Science][Medline]
17. Klausen KP, Scharling H, Jensen G, et al. New definition of microalbuminuria in hypertensive subjects: association with incident coronary heart disease and death. Hypertension (2005) 46:33–37.[Abstract/Free Full Text]
18. Wang TJ, Evans JC, Meigs JB, et al. Low-grade albuminuria and the risks of hypertension and blood pressure progression. Circulation (2005) 111:1370–1376.[Abstract/Free Full Text]
19. Stuveling EM, Bakker SJ, Hillege HL. PREVEND Study Group. C-reactive protein modifies the relationship between blood pressure and microalbuminuria. Hypertension (2004) 43:791–796.[Abstract/Free Full Text]
20. Schmieder RE, Messerli FH, Garavaglia GE, et al. Salt intake as a determinant of cardiac involvement in essential hypertension. Circulation (1988) 78:951–956.[Abstract/Free Full Text]
21. du Cailar G, Ribstein J, Daures JP, et al. Sodium and left ventricular mass in untreated hypertensive and normotensive subjects. Am J Physiol (1992) 263:H177–H181.[Web of Science][Medline]
22. Liebson PR, Grandits GA, Prineas RJ, et al. Echocardiographic correlates of left ventricular structure among 844 midly hypertensive men and women in the treatment of mild hypertension study (TOMHS). Circulation (1993) 87:476–486.[Abstract/Free Full Text]
23. Swaye PS, Gifford RW, Berretoni JN. Dietary salt and hypertension. Am J Cardiology (1972) 29:33–38.[CrossRef][Web of Science][Medline]
24. du Cailar G, Ribstein J, Mimran A. Dietary sodium and target organ damage in essential hypertension. Am J Hypertens (2002) 15:222–229.[CrossRef][Web of Science][Medline]
25. Dhingra R, Pencina M, Benjamin E, et al. Cross-sectional relations of urinary sodium excretion to cardiac structure and hypertrophy. The Framingham heart study. Am J Hypertens (2004) 17:891–896.[Web of Science][Medline]
26. Fox CS, Larson MG, Hwang SJ, et al. Cross-sectional relations of serum aldosterone and urine sodium excretion to urinary albumin excretion in a community-based sample. Kidney Int (2006) 69:2064–2069.[CrossRef][Web of Science][Medline]
27. Franklin SS, Khan SA, Wong ND, et al. Is pulse pressure useful in predicting risk for coronary heart disease? The framingham heart study. Circulation (1999) 100:354–360.[Abstract/Free Full Text]
28. du Cailar G, Mimran A, Fesler P, et al. Dietary sodium and pulse pressure in normotensive and essential hypertensive subjects. J Hypertension (2004) 22:697–703.[CrossRef][Web of Science][Medline]
29. Avolio AP, Fa-Quan D, Wei-Qiang L, et al. Effect of aging on arterial distensibility in populations with high and low prevalence of hypertension: comparison between urban and rural communities in China. Circulation (1985) 71:202–210.[Abstract/Free Full Text]
30. Avolio AP, Clyde KM, Beard TC, et al. Improved arterial distensibility in normotensive subjects on a low salt diet. Arteriosclerosis (1986) 6:166–169.[Abstract/Free Full Text]
31. Alderman MH, Cohen H, Madhavan S. Dietary sodium intake and mortality: the National Health and Nutrition Examination Survey (NHANES I). Lancet (1998) 351:781–785.[CrossRef][Web of Science][Medline]
32. Cohen HW, Hailpern SM, Fang J, et al. Sodium intake and mortality in the NHANES II follow-up study. Am J Med (2006) 119:275–282.
33. Shimazu T, Kuriyama S, Hozawa A, et al. Dietary patterns and cardiovascular disease mortality in Japan: a prospective cohort study. Int J Epidemiol (2007) 36:600–609.[Abstract/Free Full Text]
34. He J, Ogden LG, Vupputuri S, et al. Dietary sodium intake and subsequent risk of cardiovascular disease in overweight adults. JAMA (1999) 282:2027–2034.[Abstract/Free Full Text]
35. Tuomilehto J, Jousilahti P, Rastenyte D, et al. Urinary sodium excretion and cardiovascular mortality in Finland: a prospective study. Lancet (2001) 357:848–851.[CrossRef][Web of Science][Medline]
36. Hu G, Jousilahti P, Peltonen M, et al. Urinary sodium and potassium excretion and the risk of type 2 diabetes: a prospective study in Finland. Diabetologia (2005) 48:1477–1483.[CrossRef][Web of Science][Medline]
37. Appel LJ, Espeland MA, Easter L, et al. Effects of reduced sodium intake on hypertension control in older individuals: results from the Trial of Nonpharmacologic Interventions in the Elderly (TONE). Arch Intern Med (2001) 161:685–693.[Abstract/Free Full Text]
38. Cook NR, Cutler JA, Obarzanek E, et al. Long term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention (TOHP). BMJ (2007) 334:885–892.[Abstract/Free Full Text]
39. Nickenig G, Strehlow K, Roeling J, et al. Salt induces vascular AT1 receptor overexpression in vitro and in vivo. Hypertension (1998) 31:1272–1277.[Abstract/Free Full Text]
40. Gonzalez M, Lobos L, Castillo F, et al. High-salt diet inhibits expression of angiotensin type 2 receptor in resistance arteries. Hypertension (2005) 45:853–859.[Abstract/Free Full Text]
41. Takeda Y, Yoneda T, Demura M, et al. Sodium-induced cardiac aldosterone synthesis causes cardiac hypertrophy. Endocrinology (2000) 141:1901–1904.[Abstract/Free Full Text]
42. Cordaillat M, Rugale C, Casellas D, et al. Cardiorenal abnormalities associated with high sodium intake: correction by spironolactone in rats. Am J Physiol (Regul Integr Comp Physiol) (2005) 289:R1137–R1143.[Abstract/Free Full Text]
43. Laffer CL, Bolterman RJ, Romero JC, et al. Effect of Salt on isoprostanes in salt-sensitive essential hypertension. Hypertension (2006) 47:434–440.[Abstract/Free Full Text]
44. Fang Y, Mu JJ, He LC, et al. Salt loading on plasma asymmetrical dimethylarginine and the protective role of potassium supplement in normotensive salt-sensitive asians. Hypertension (2006) 48:724–729.[Abstract/Free Full Text]

Received for publication: 12. 6.07
Accepted in revised form: 29. 2.08

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