LOW SODIUM INTAKE

INCREASE
MORTALITY

Salt reduction benefits :

myth or reality?
Sodium and health policy :
population-wide reductions in
sodium intake.
1) Is there a normal or healthy range?
2) Current intakes are excessive;
3) The healthy range must be below
current intakes;
4) Human intake is dictated by the
sodium content of the food supply;
5) Lower sodium intake is always better

Symposium "Beyond Blood Pressure: New Paradigms in Sodium Intake Reduction and Health Outcomes
29 April 2014 at the ASN Scientific Sessions and Annual Meeting at Experimental Biology 2014;

Is there a normal or healthy range?

24-h urinary sodium excretion worldwide. Data from 62 survey sites in 33 countries; n = 19,151 individuals.
IJE, International Journal of Epidemiology; IS, Intersalt Data from BMJ 1988; UNaV, urinary sodium excretion
value.

3700mg/day -consistent across study year, age, gender, and race,

culinary habits, climate

Physiologic relation of the 24-h UNaV to PRA predicts mean sodium intake.
PRA, plasma renin activity; UNaV, urinary sodium excretion value

-correlated with PRA/24-h UNaV 3550mg/day

Various stimulatory and inhibitory signals act on the brain to regulate sodium appetite. CNS, central
nervous system; Osm, osmolality.

human sodium intake is a physiologic variable

1 teaspoon salt = 2,300 mg sodium

The Center for Nutrition Policy
and Promotion // KDIGO recomandation

2) Current intakes are excessive

3) The healthy range must
be below current intakes

1500mg

2300 mg

2600 mg

3400 mg

3700 mg

4800mg

Lower sodium intake is always better

 The main finding : those consuming more or less sodium were at

increased risk of both ACM and CVD.
no difference in outcomes between the higher and lower sodium intake
groups within the usual range of sodium intake.
J/Ushaped relation of sodium intake to health outcomes

Estimated 24 h urinary excretion of sodium and composite

of cardiovascular death, stroke, myocardial infarction, and
hospitalization for congestive heart failure.

EPIDEMIOLOGICAL FACTS:

INTERSALT (International Study of Salt) study failed to document any

association of salt intake with either the actual BP of a population or the
prevalence of hypertension
ONTARGET(Ongoing Telmisartan Alone and in Combination With
Ramipril Global Endpoint Trial) and TRANSCEND(Telmisartan
Randomized Assessment Study in ACE Intolerant Subjects With
Cardiovascular Disease) trials : J-shaped association between urinary
sodium excretion and cardiovascular events

Institute of Medicine: USA expert committee:

the relation between sodium excretion and blood pressure was
positive but nonuniform:

the

strong in participants with high sodium excretion

modest in those in the moderate range

Nonsignificant in those with low sodium excretion.

A very small proportion of the worldwide population consumes a

low-sodium diet and sodium intake is not related to blood
pressure in these persons, calling into question the feasibility
and usefulness of reducing dietary sodium as a populationbased strategy for reducing blood pressure.

The

Prospective Urban Rural Epidemiology (PURE) study

provides new evidence about the association between sodium and
potassium intake and blood pressure, death, and major
cardiovascular events

Which one is the first:

Hypertension or high sodium intake?
Sodium intake is often increased in disease with compromised
renal perfusion : congestive heart failure and renal disease,
including diabetes.
CHF, CKD: PRA/angiotensin II to increase renal
perfusion and suppress PRA, and the subsequent generation of
angiotensin II and its pathologic impact on the heart and
vasculature a neural-driven increase in sodium intake

Causative or secondary compensatory response mechanism

abrogating that compensatory response by restricting salt
intake enhances progression

CARDIAC FAILURE
restriction increased the risk of all-cause mortality in patients with congestive
heart failure.

Sodium

with low urinary sodium excretion had an increased risk of

cardiovascular mortality and hospitalization for congestive heart failure.
Normal-sodium diet improves outcome, and sodium depletion has detrimental renal
and neurohormonal effects with worse clinical outcome in compensated CHF patients.
Patients

Taylor RS, Ashton KE, Moxham T, Hooper L, Ebrahim S.

Reduced dietary salt for the prevention of cardiovascular disease: a
meta-analysis of randomized controlled trials (Cochrane Review).
Am J Hypertens. 2011;24(8):843-853.
ODonnell MJ, Yusuf S, Mente A, et al. Urinary sodium
and potassium excretion and risk of cardiovascular events. JAMA.
2011;306(20):2229-2238.
Salvatore Paterna. Normal-sodium diet compared with
low-sodium diet in compensated congestive heart failure: is sodium an old enemy or a new friend?

KIDNEYS
the benefits of reninangiotensinaldosterone
system blockade might be reduced by adherence
to a low-sodium diet
controlled intervention studies in animals :
vigorous restriction of dietary sodium+ RAAS
blockade profound interstitial damage both
in healthy rats and nephrotic rats.

Hamming I, Navis G, Kocks MJ et al. ACE inhibition has adverse

renal effects during dietary sodium restriction in proteinuric and
healthy rats. J Pathol 2006; 209: 129139

DIABETES
Finnish multicenter FinnDiane Study( evaluating 2,807 adults
with type 1 diabetes); inverse relationship between
sodium intake and development of end stage renal
disease.
In patients with type 2 diabetes, lower 24-h urinary sodium
excretion was paradoxically associated with increased all-cause
and cardiovascular mortality.

Mortality was inversely related to sodium intake: for every increase in

sodium excretion of 100mmol/d, the associated all-cause mortality
decreased by 28%.

Thomas MC, Moran J, Forsblom C, et al. The association between dietary sodium intake, ESRD, and all-cause mortality in
patients with type 1 diabetes. Diabetes Care. 2011;34(4):861-866.
Ekinci EI, Clarke S, Thomas MC, et al. Dietary salt intake and mortality in patients with type 2 diabetes. Diabetes Care.
2011;34(3):703-709.

METABOLISM

Sodium reduction resulted in:

significant increase in plasma renin, plasma

aldosterone, plasma adrenaline and plasma
noradrenaline
2.5% increase in cholesterol
7% increase in triglyceride

the slight reduction in blood pressure might be

overshadowed by these antagonistic effects

These effects were stable in studies lasting for 2

weeks or more.

Jaime L.ClarkPossible deleterious hormonal changes associated with low-sodium diets, Oxford
University Press on behalf of the International Life Sciences Institute

GERIATRIC PACIENTS
altered homeostatic systems involved in the
regulation of fluid balance including thirst
perception that govern fluid intake, the kidney,
regulation of secretion of arginine vasopressin or
antidiuretic hormone, atrial natriuretic hormone,
and the reninangiotensinaldosterone system
Low sodium intake + age-associated impaired
renal sodium-conserving ability sodium
depletion with hyponatremiamore falls and
fractures and a decrease in cognitive abilities.

Myron Miller :Hyponatremia in the Elderly: Risk Factors, Clinical Consequences, and Management,
Consultant Primary Care Physician Journal, mars 2015

CONCLUSIONS
many of the assumptions underlying the genesis of
sodium reduction health policy are not supported
by data from basic science, clinical interventions;
Further research is needed to better understand
the long-term effects of extreme sodium
restriction;
Ideally, recommendations for each patient should
be tailored based on individual risk factors and
comorbid conditions;
There is an increased risk of all causes mortality,
cardiovascuar events related to low sodium diets in
general population;

Eat less salt

or not