Sodium is the most abundant extracellular cation and therefore pivotal in determining fluid balance. At the beginning of life, a positive sodium balance is needed to grow. Newborns and preterm infants tend to lose sodium via their kidneys and therefore need adequate sodium intake. Among older children and adults, however, excessive salt intake leads to volume expansion and arterial hypertension. Children who are overweight, born preterm, or small for gestational age and African American children are at increased risk of developing high blood pressure due to a high salt intake because they are more likely to be salt sensitive. In the developed world, salt intake is generally above the recommended intake also among children. Although a positive sodium balance is needed for growth during the first year of life, in older children, a sodium- poor diet seems to have the same cardiovascular protective effects as among adults. This is relevant, since 1): a blood pressure tracking phenomenon was recognized 2); the development of taste preferences is important during childhood; and 3) salt intake is often associated with the consumption of sugar-sweetened beverages (predisposing children to weight gain).
22
Abstract
Sodium is the most abundant extracellular
cation and therefore pivotal in determining
fluid balance. At the beginning of life, a po-
sitive sodium balance is needed to grow.
Newborns and preterm infants tend to lose
sodium via their kidneys and therefore need
adequate sodium intake. Among older child –
ren and adults, however, excessive salt in –
take leads to volume expansion and arterial
hypertension. Children who are overweight,
born preterm, or small for gestational age
and African American children are at incre –
ased risk of developing high blood pressure
due to a high salt intake because they are
more likely to be salt sensitive. In the deve –
loped world, salt intake is generally above
the recommended intake also among child –
ren. Although a positive sodium balance is
needed for growth during the first year of
life, in older children, a sodium- poor diet
seems to have the same cardiovascular
protective effects as among adults. This is
relevant, since 1): a blood pressure tracking
phenomenon was recognized 2);
the
development of taste preferences is impor –
tant during childhood; and 3) salt intake is
often associated with the consumption of
sugar-sweetened beverages (predisposing
children to weight gain).
Introduction
The words salus (Latin for health\b and salub-
ris (healthy\b underscore the role of salt in
ancient Rome, where salt was regarded as a
symbol of health and prosperity, likely becau –
se of it s role in foo d pr eser vation
1\b. In the eyes
of Homer, salt represented a divine subs-
tance
2\b, whereas it was a cornerstone of daily
life in the Jewish–Christian tradition (Esdra
6,9; Esdra 7,22; Gb 6,6; Lv 2, 13; 2Re 2,21; Mt
5,13\b. Historically, salt was a precursor of
coins (e.g., salt tax, 1Mac 10,29\b, and it led to
the discovery of shipways and adventurous
trips. In ancient Rome, soldiers were paid a specific quantity of salt
(salarium) rather than
gold or coins. Thus, salt was an important
currency. The relevance of salt is also reflec –
ted in the name of numerous cities including
Salzburg (Austria\b, Langensalza (Germany\b,
Sandwich (England\b, and Saltcoats (Scot –
land\b. At the beginning of the late modern
p er io d , the s alt t a x was imp or t ant ; in f act , s alt
tax officers were decapitated during the
French Revolution
3\b. In several cultures
around the world, salt (a white substance\b is
a symbol of the imperishable; it was an emb –
lem of immortality and loyalty, which is reflec –
ted by the sharing of bread and salt with a guest, a tradition that remains alive in Slavic
countries
3\b. Salt is the spice
par excellence
because it provides taste and flavor to food.
Finally, consider the Latin expression cum
grano salis (literally, with a grain of salt\b,
which means with common sense. An abun-
dance of literature has appeared about the
role of salt on bloo d pr es sur e, throughout this
review we consider and highlight some key
papers focusing on this problem in childhood.
Physio\bogica\b aspects
Sodium, the most abundant extracellular ca-
tion, is pivotal in determining fluid balance 4\b.
The total sodium content of the adult human
body is ~
80
mmol/kg of fat-free body
weight
5\b; this proportion is higher in new –
borns, infants, and children 6\b , 7\b . Fluid and so –
dium balances play a central role in regulating
blood pressure and, potentially, in the deve-
lopment of arterial hypertension. Several
factors modulate salt handling, such as –
among others – acti
va
tion of the sympathetic
nervous system, hyperinsulinemia, hypercal –
Salt intake in children and its
consequences on blood pressure
Sebastiano A. G. Lava, Mario G. Bianchetti, Giacomo D. SimonettiReceived: 29 March 2014/Revised: 23 July 2014/Accepted: 24 July 2014 © IPNA2014
Reproduced from Pediatr Nephrol, 2014 Aug 17 ISSN 0931- 041X
With kind permission of Springer Science + Business media
Fig 1: Excess sodium modulates lymphangiogenesis, and osmotically inactive sodium accumu –
lates in the skin interstitium, binding proteoglycans. Excess sodium recruits macrophages, and
subsequently activates within subcutaneous macrophages (cells with blue nucleus) a trans-
cription factor, tonicity-enhanced binding protein, which in turn induces the production of the
angiogenic protein vascular endothelial growth factor-C. Vascular endothelial growth factor-C
stimulates lymphatic vessel (red) growth and creates a new fluid compartment, which buffers
the increased body sodium (yellow) and ameliorates the tendency to excess body fluid linked
with excess salt intake. Adapted with permission from15\b.
1Prof. ffRPofTff.aTb
1Prof. PRTaPR. Rbi
23
cemia, acid-base balance 8\b, hyperaldostero-
nism 8\b , 9\b , leptin 10 \b, genetic background, and
maybe also circulating cardioglycosides 11 \b.
Most of these systems ultimately work
through the kidney, with the renin-aldostero –
ne-angiotensin system playing a pivotal role
in fluid and sodium homeostasis. This impor –
tance is suggested by several monogenetic
hypertensive diseases
12 \b. Furthermore, it was
demonstrated via transplantation experi –
ments in both rats and humans that essential
hypertension resolved after bilateral nephrec –
tomy and kidney transplantation
13 \b.
Newer data suggest that an extrarenal system
may play a role in sodium handling. Elegant
experiments by Titze and coworkers propose
that so dium can b e stor ed on negati vely char -ged glycosaminoglycans in the skin interstiti
–
um, where it becomes osmotically inactive
14 \b.
Thus, the skin interstitium might act as a ne –
gatively charged capacitor and fluid-buffering
sys tem ab l e to s tor e s o dium w ithout comm en –
surate water retention. In this way, it could
blunt accumulation of excess body fluid (and
the resultant high blood pressure\b following
high salt intake
14 \b. Actually, sensing the accu –
mulation of sodium cations, macrophages
might be recruited and subsequently release
vascular endothelial growth factor C (VEGF-
C\b, which stimulates hyperplasia of the cuta –
neous lymph capillary network, inducing local
clearance of skin electrolytes ( F i g . 1)
14 \b , 15 \b .
These mechanisms might be impaired or
overwhelmed in salt-sensitive hypertensive
individuals. At this time, it is not known which pathways may be involved. Furthermore,
nothing is known about these proposed pa-
thways in children or about possible develop
–
mental expression of such mechanisms.
E\bectro\bytes and fluid ba\bance
among newborns and infants
A p ositi ve so dium balance is ne ces s ar y at the
beginning of life. Although ~
30
–50
% o
f the
adult body sodium content resides in the
skeleton, this proportion is much smaller
among infants and small children. Thus, a
positive sodium balance is needed during
development to build the skeleton and p er mit
growth. Since infancy constitutes the most
important and rapid growth period of life, in –
fants need ~
95
–115 mmol sodium per kilo –
gram of weight gain
6\b. While urine production
begins at ~
9–
12 gestational weeks, nephro –
genesis is not complete until 35–36 gestatio –
nal weeks
16 \b , 17 \b . Glomerular filtration rate
(GFR\b doubles during the first 2 weeks of
life
17 \b, and several tubular transport mechanis –
ms mature after birth 18 \b.
The concentration ability of term neonates is
limited, with a maximal urine osmolality of
~
70
0–800 mOsm/kg H
2O16 \b. Preterm new-
borns show lower concentration abilities
( 60 0 –70 0 m Osm/k g H
2O \b . O n the other hand ,
they also have a lower GFR and therefore a
reduced ability to excrete water.
Due to tubular immaturity, sodium is often
lost during the first 2–3 weeks of life, thereby
leading to a negative sodium balance (i.e., the
physiological contraction of extracellular vo –
lume after birth and compensation for the
transepithelial hypotonic water lost\b
17 \b. Never –
theless, the sodium balance is generally
maintained in term newborns because the
fractional sodium excretion (FE
Na\b stabilizes
at ~
1 % (
or even lower\b near the third day of
life. In addition, plasma concentrations of
renin, angiotensin, and aldosterone are high
in newborns, thereby shifting the sodium ba-
lance in a positive direction. Plasma concen –
trations of these mediators decrease during
the first weeks of life, in parallel with the
maturation of several tubular transporters
16 \b.
Experimental data have shown that sodium
plays a role in stimulating growth. The side
effects of sodium deprivation were shown at
a cell proliferation level in bones and nerves.
Chronic sodium depletion retards growth in
both experimental rats and humans
17 \b; thus,
due to the increased losses, preterm infants
Fig 2: Sodium balance among preter m infants bor n at 27–34 gestational weeks. The red histo –
g r ams show the sp ont aneous cour se of so dium balance among nor mally fed , other w ise healthy,
preterm infants. The green histograms depict the course of sodium balance among preterm
infants who received a sodium supplementation of 4–5 mmol/kg/day. Adapted with permission
f r o m19 \b .
Age
(years) Mean daily salt
i n t a k e ( g /d a y )Range
( g /d a y )Recommended
daily salt intake
( g /d a y )
< 1 0.50 . 4 –1 . 3< 1
1–5 43.3 – 4.92
5 –1 0 63 . 7– 8 .14
10 –20 86 . 7–11 . 05
Table 1: Mean and recommended salt intake at different ages.
To convert a gram of salt to a millimol of sodium, divide by 0.058 g/mmol.
To convert from a gram of salt to a gram of sodium, multiply by 0.3972\b, 18\b, 20\b.
1Prof. ffRPofTff.aTb
1Prof. PRTaPR. Rbi
24
should be supplemented with sodium. In fact,
salt lost is greater among preterm and low-
birth-weight (LBW\b infants
16 \b , 17 \b , placing these
child
re
n at risk of developing associated
ne
gative salt balances and hyponatremia
(F
ig. 2) .
A seminal study demonstrated that preterm
infants supplemented with 4–5 mmol/kg per
day of sodium during the first 2 weeks of life
reached a positive sodium balance more ra-
pidly, lost less weight postnatally, and regai-
ned birthweight more quickly compared with
a control group of nonsupplemented infants
(Fig. 2) . Interestingly, the effect of this inter-
vention on infant weight remained significant
after supplementation ceased
19 \b. In contrast,
full-term infants fed breast milk receive
~
1 m
mol/kg per day of sodium, which is
enough for an equilibrated growth
6\b. Sodium
intake < 1 mmol/kg per day might lead to
hyponatremia and growth retardation and
should therefore be avoided.
Sa\bt intake during chi\bdhood
Due to regulation mechanisms, the minimal
sodium requirement under constant condi -
tions (i.e., after development\b is low: in fact,
~
0.
1 mmol Na
+/10 0 kcal might b e enough. At
the other extreme, humans can tolerate up to
10 mmol Na
+/100 kcal without experiencing problems
6\b. Upper limits for the recommen
-
ded daily salt intake are given in Ta b l e 1 .
According to data from 1997, 4-year-olds in
the UK consumed 4.7 g/day of salt (i.e., 81.0
mmol/day\b, whereas 18-year-olds ingested
6.8 g/day (i.e., 117 mmol/day\b
21 \b. Similar data
were recently published regarding the US:
8- to 18-year-olds had a mean intake of 8.6
g/day (i.e., 148 mmol/day\b. In addition, that
study noted that salt intake increased with
age
22\b. Furthermore, salt intake was higher
among boys than girls, among normal-weight
than over weight par ticipant s , and among non -
Hispanic white than Hispanic-white and dark-
skinned participants.
Ta b l e 1 summarizes data from several sour -
ces regarding actual salt int ake among child -
ren and compares it with agerecommended
salt intakes. The variability among age, sex,
and the single studies is considerable. Salt
intake increases with age due to differences
in total food consumption and food cho -
ices
23 \b. In summary, salt intake is generally
≥
5.
8 g/day (i.e., 100 mmol/day\b starting at
~
5 y
ears of age and increases by ~
25
0 mg/
day per year (i.e., 4.3 mmol a day per year\b
23 \b.
Very recent data appear to confirm these
results
20 \b. Salt intake studies are difficult to conduct.
Food diaries, 24-h urinary sodium, overnight
urinary sodium, and spot urinary sodium/
creatinine ratio, while being adequate assess-
ment s of compliance w ith dif fer ent salt- int ake
regimens, are unreliable in accurately asses-
sing absolute dietary salt intakes
24 \b. In parti-
cular, food diaries and urine measurements
tend to under estimate salt int ake
23 \b. Available
data must therefore be interpreted with cau -
tion. Importantly, a tracking phenomenon was
identified with respect to salt intake; in other
words, a taste habituation is present that
generates dietary routines
25 \b , 26 \b . Interestingly,
boys eat ~
20 m
mol/day more salt than girls,
and dark-skinned children eat ~
15
mmol/day
more salt than white children
23 \b. Adults con-
sume ~
70
–80
% o
f their salt intake from ma-
nufactured foods, snacks, and restaurant and
fast-food meals, whereas only ~
10
% occurs
naturally in foods and another 10
% c
omes
from discretionary use at home (added at the
table or during cooking \b
23 \b , 27 \b . Childhood data
are limited; however, they seem to globally
reflect the adult data
23 \b. Interestingly, cereals
are the largest contributor to dietary salt in-
take ( ~
40 %\b
, followed by meat products
( ~
20 %\b a
nd milk products ( ~
1 0 %
\b
20 \b , 23 \b .
Effects of sa\bt on b\bood pressure
among chi\bdren and ado\bescents
Among older children, excessive salt intake
leads to the same complications that are
known among adults: volume expansion and
arterial hypertension. Several epidemiologi -
cal, observational and population studies
suggest that salt intake is associated with
hypertension in children
24\b , 28 \b . As stated abo -
ve, salt- int ake studies ar e dif ficult to conduct .
Nevertheless it is possible to analyze the re -
lative changes in salt intake among children
(using any of the methods listed above\b in
interventional studies
24 \b.
T he pioneer ing study of a salt int ake r e duction
campaign was performed in Japan in the
1950 s
24 \b , 29 \b . T his campaig n was able to r e duce
mean salt intake by ~
1.
5 g/day (i.e., 26
mmol/day\b. The effects of this intake reduc-
tion were noted among school children over
more than 15 years. Several observational
studies have not found a significant associa-
tion between salt and blood pressure; howe -
ver, they present various methodological
problems
24 \b. In fact, most high-quality studies
have demonstrated a significant association
between salt intake and hypertension among
Fig 3:
Odds ratios (ORs\b for developing high blood pressure among 6,235 US children 8–18
years old. Children were divided into quartiles based on their sodium intake. The Y-axis shows
ORs for developing high bloo d pr es sur e ( pr ehy p er tension or hy p er tension \b . T he blue bar s depict
ORs for all studied participants, and the red bars show the ORs for the subgroup (37.1
%\b
of
overweight and obese children. This graph was developed based on data from Yang et al.22\b.
1Prof. ffRPofTff.aTb
1Prof. PRTaPR. Rbi
25
children 24 \b. An interesting study was perfor-
med based on the National Diet and Nutrition
Survey for Young People program undertaken
in 1997 in the UK. This study showed that an
increase in salt intake of 1 g/day (i.e., 17.2
mmol/day\b increased systolic blood pressure
(SBP\b by 0.4 mmHg
21 \b among 4- to 18-year-
olds. A meta-analysis by He and McGregor
reviewed ten controlled studies (nine of which
were randomized\b among children and adole -
scents and three controlled studies among
infants
24 \b. It is interesting to note that alt-
hough many studies have been conducted on
this topic, the authors of that study found only
13 controlled trials. Furthermore, in several
studies, there were important flaws limiting
their credibility. The authors calculated the
percentage change in salt intake using the
qualitatively best available technique: 24-h
urinary sodium, overnight urinary sodium,
spot urinary sodium/creatinine ratio, or food
diary. These measures were used to index
salt-intake reduction. The child and adole -
scent studies included in the meta-analysis
comprised a total of 966 participants, with a
median age of 13 years (range 8–16 years\b
and a median salt-intake reduction duration 4
of weeks (range 2 weeks to 3 years\b. Median
salt intake reduction was 42
%
(interquartile
range (IQR\b 7–58
%\b
; this reduction was ac-
companied by reductions in systolic blood
pressure (SBP (−1.17 mmHg, 95
% c
onfidence
interval (CI\b −1.78 to −0.56 mmHg, p < 0.001\b]
and diastolic blood pressure (DBP\b (−1.29
mmHg, 95
% C
I −1.94 to −0.65 mmHg,
p< 0.0001\b. After excluding the only nonran-
domized study, results were similar, and sig-
nificance was maintained: SBP −0.93 mmHg
(95
% C
I −1.66 to −0.20, p=0.01\b, DBP −1.07
mmHg (95
% C
I −2.00 to −0.14 mmHg,
p= 0.02\b. Diet adherence was low in two stu -
dies (< 5
% d
ifference between two diet
groups\b; thus, the authors performed a suba -
nalysis of the studies with relevant adherence.
Results were in the same range, and the sig-
nificance wassimilar (SBP −1.18 mmHg, 95 %
CI −1.82 to −0.55 mmHg, p=0 .0003; DBP
−1.20 mmHg, 95
% C
I −1.86 to −0.54 mmHg,
p= 0.0003 \b . Study heterogeneit y was not sig -
nificant, and no evidence of publication bias
was detected
24 \b.
The three infant studies comprised 551 parti -
cipants. Due to the low reliability of DBP mea -
surements during infancy, the authors only
examined SBP. Median duration of reduced salt
intake was 20 weeks (range 8 weeks to 6 mon -
ths\b, and median salt intake reduction was 54
% (
IQR 51–79
%\b
. These results were accompa
-
nied by an SBP reduction of −2.47 mmHg (95
%
C
I −4.00 to −0.94 mmHg, p<
0 . 01 \b .
Ro\be of potassium
T he daily so dium int ake of hy p er tensi ve child -
r en should b e decr eased , and their p ot as sium
intake should be adequate
28 \b , 30 \b . Evidence
suggests that this dietary intervention has
positive short- and long-term effects on blood
pressure. In fact, there is a substantial body
of literature discussing various dietary and
lifestyle interventions possibly capable of
reducing blood pressure independently of salt
restriction
10 \b. In particular, a diet rich in fruits
and vegetables, low-fat dairy products, and
low saturated and total fat (the so - called
Dietary Approaches to Stop Hypertension,
DASH, diet\b was able to decrease blood pres -
sur e by 5.5/3.0 mmHg
31 \b. Interestingly, reduc-
tion in salt intake and the DASH diet lowered
blood pressure significantly, with greater ef-
fects in combination than singly
32\b.
T he ef fect of maint aining su f ficient p ot as sium
intake is
mo
st likely smaller than that of
maintaining a lower sodium intake
28 \b. A high
potassium intake and a low Na +/K + ratio ap -
pears to positively affect the physiological
rise of blood pressure in childhood, resulting
in smaller blood pressure slopes
33\b. Finally, a
study among normotensive African American
adolescents showed that potassium supple -
mentation reversed nondipper patients into
physiological dipper behavior
34\b.
Chi\bdren at increased
risk for sa\bt sensitivity
Sa
lt sensitivity is defined as the significant
aug ment ation of ar ter ial bloo d pr es sur e follo -
wing increased salt intake. Overweight child-
ren
9 \b , 22 \b , 28 \b , 3 5 \b , childr en w ho wer e b or n pr eter m
or small for gestational age (SGA\b 36\b, and
African American children 28 \b are at an incre -
ased risk of developing high blood pressure
when exposed to high salt intake, because
these groups present higher prevalence of
salt sensitivity. Overweight children are the
most relevant risk group because they re-
present an intervention population (e.g., via
weight-reduction campaigns\b. Furthermore,
the prevalence of childhood obesity has inc-
reased
35\b , 37\b . A recent study performed in the
USA evaluated the effect of salt on blood
pressure among 8- to 18-year-olds, distingu -
ishing b et ween nor mal - weight and over weight participants
22\b. The prevalence of overweight
and obesity (37.1
%\b
and the prevalence of
prehypertension or hypertension (14.9
%\b
were high. The authors of that study calcula -
ted that participants’ SBP increased by ~
1
mm
Hg for each gram of increased sodium
intake per day (i.e., 43.5 mmol/day\b, and this
increase was ~
1.
3 mmHg g r eater among over-
weight and obese participants (1.5 mmHg\b
compared with normal-weight participants
( ~
0.2
mmHg\b
22\b. However, DB P was not sig ni -
ficantly associated with sodium intake. The
authors subdivided participants into salt-in -
take quartiles, and comparison between the
lowest and highest quartiles revealed an ad -
justed hypertension risk of 1.98. Results of
the subanalysis compared normal-weight and
over weight childr en and wer e even mor e inte -
resting: the adjusted risk among normal-
weight participants was 1.15, whereas it was
3.51 among overweight and obese children
(Fig. 3) . The risk for (pre- \b hypertension incre -
ased by 35
% f
or each additional gram of sodi -
um per day among normal-weight participants
and by 74
% a
mong overweight and obese
children. Finally, a relative excess risk due to
interaction (RERI\b was identified, which me -
ans that these risk factors were synergistic.
Sp e ci fically, they not only incr ease d the global
risk by their respective factors but also led to
an even greater risk due to their concomitant
presence and interaction. The pathophysiolo -
gical mechanism that develops salt sensitivity
in obese children is likely due (among other
possibilities\b to insulin resistance and hy -
perinsulinemia, which activate the renal sym -
pathetic nervous system that causes vasocon -
striction and reduces renal blood flow,
thereby activating the renin-angiotensin-
al
dosterone system and inducing salt sensiti -
vity
9\b , 38\b , 39\b .
The second risk group comprises children
born preterm or with low birth weight (LBW\b.
One study found an increased salt-sensitivity
risk among children who were of low birth
weight (LBW\b or small for gestational age
(SGA\b
36\b. The salt-sensitivity prevalence at
7–15 years of age was 37
% a
mong LBW and
47
% a
mong SGA children. These rates were
much greater than one might expect in the
general adult population. Similar results were
found among adults
40\b.
People at increased cardiovascular risk (e.g.,
African Americans, patients with hypertensi -
on, and people with family history of hyper-
tension\b are more likely to have a salt sensiti
1Prof. ffRPofTff.aTb
1Prof. PRTaPR. Rbi
26
vit y than control people 28 \b. In a well- designed
study, sodium retention among African Ame -
rican and white adolescent girls fed low- and
high-sodium diets was compared. African
American adolescent girls showed a higher
retention of sodium compared with Caucasian
gir ls. T hus , a dif fer ent t y p e of so dium handling
might be (partially\b responsible for the greater
salt-sensitivity prevalence among African
Americans
41 \b. In fact, despite the sodium re-
tention, neither blood pressure nor weight
increased, so that the retained sodium had to
reside in a nonextracellular compartment
41 \b.
The authors speculated that this compart -
ment is the skeleton
41 \b, but in light of the ne-
wer findings from Titze and colleagues, it is
tempting to assume that this might have been
the skin interstitium
14 \b.
Tracking and programming
The deleterious effect of a high salt intake is
not limited to childhood; rather, it has long-
lasting effects on blood pressure
26\b. High
blood pressure in childhood predisposes to
hypertension in adulthood and increases the
risk of developing cardiovascular disease and
premature death
22\b, 42\b . Animal models suggest
that salt intake during the first years of life
might have a programming effect on blood
pressure
24 \b , 43 \b . In other words, transitory salt
exposure during the first years of life might
lead to a permanent increase in blood pressu -
re, even when salt intake decreases later in
life. In a double-blind randomized trial perfor -
med almost 30 years ago among 476 newborn
infants divided into low-sodium-diet ( n=231 \b
and normal-sodium-diet ( n=245\b groups, an
association was found between salt intake
and blood pressure during the first 6 months
of life; specifically, a progressive increase in
bloo d pr es sur e was obser ved among b oth diet
groups across each month of observation
44\b.
Of the 476 children studied, 167 were recrui -
te d for a follow - up as ses sment 15 year s later.
SBPs of those fed low-salt diets during their
first 6 months of life were significantly lower
(−3.6 mmHg, 95
% C
I −6.6 to −0.5 mmHg,
p= 0.02\b, although the dietary salt intake did
not significantly differ between groups at 15
year s of age
45\b. T his is sue, however, is contr o -
ver sial, since the liter atur e of fer s var iable and
limited results
46\b , 47\b . In particular, studies de -
nying an association are problematic because
they present several flaws limiting their inter -
pretation.
Re\bevance for pub\bic hea\bth
Data regarding salt intake in childhood are
relevant, particularly from a public health
perspective. First, high blood pressure is an
important cause of disease burden measured
as Disability Adjusted Life Years (DALY\b
48\b.
Second, a blood-pressure-tracking effect was
documented: children with hypertension of -
ten mature into adults with hypertension.
Third, risk of hyper tension appears to be inc -
reased with higher sodium intake in child-
hood. Fourth, taste preferences are imprinted
during childhood: children who typically con -
sume a significant amount of salt are likely to
prefer salty meals as adults
25\b. In fact, salty
snacks consumed during childhood might
suppress the ability to taste salt, thereby
programming salty meal consumption during
adulthood
24 \b.
Among Australian children, salt intake led to
an increased fluid intake ( r=0.42, p<0 . 0 01 \b :
each additional gram of salt consumed was
associated with an additional 46-g intake of
fluids per day. Because two thirds of these
children drank sugar-sweetened beverages,
their sugar intake increased with their salt
intake ( r=0.35, p<0.001\b: each additional
gram of salt was associated with an additional
17- g int ake of sugar- sweetene d b ever ages p er
day
49\b. In other words, adolescents who con-
sume a significant amount of salt also tend to
be overweight. Similar results were found in
Great Britain (each additional gram of salt
consumed was associated with an additional
27-g intake of sweetened beverages per
day\b
35\b. Based on these data, reducing one’s
daily salt intake might also contribute to the
prevention of obesity and overweight among
children
35\b , 49\b .
Conc\busions
Evidence indicates that reduced salt intake
benefits children. Although at the beginning
of life a positive sodium balance is required
for growth, during the first year of life, a low-
salt diet among older children seems to have
the same cardiovascularprotective effects
known among adults, particularly with re-
spect to blood pressure reduction. Whether
salt-intake reduction affects cardiovascular
outcomes remains controversial; however,
most of the literature currently suggests that
a restricted salt intake plays a preventive
role
50\b –53\b . A low-salt diet is especially impor -
tant for overweight children, those born pre -term, those born SGA, and those who have
hypertension or present nonpreventable car
-
diovascular risk factors (e.g., family history of
hypertension, African American heritage\b.
Salt intake during childhood is relevant for
public health: first, elevated blood pressure
during childhood predicts elevated blood
pressure during adulthood; second, salt in-
take increases hypertension risk in childhood;
third, taste preferences are developed during
childhood; fourth, salt intake is often associ -
ated with consumption of sugar-sweetened
beverages. Further research is needed to
identify and evaluate possible preventive in-
terventions on individual and systemic bases
during childhood.
References
1) Pickering TG (2002) The histor y and politics of salt.
J C lin Hypertens (Greenwich) 4: 226–228.
2)
Kot
chen TA, Cowley AW Jr, Frohlich ED (2013) Salt
in health and disease–a delicate balance. N Engl J
M e d 368: 1229–1237.
3)
Ri
tz E, Mehls O (2009) Salt restriction in kidney
disease–a missed therapeutic opportunity? Pedia -
tr Nephrol 24: 9–17.
4)
Hi
ll LL (1990) Body composition, normal electroly -
te concentrations, and the maintenance of normal
volume, tonicity, and acid-base metabolism. Pedi -
atr Clin N Am 37: 241–256.
5)
Fo
rbes GB, Lewis AM (1956) Total sodium, potassi -
um and chloride in adult man. J Clin Invest 35:
596–600.
6)
Fi
nberg L, Kravath RE, Hellerstein S (1993) Water
and electrolytes in pediatrics—physiology, patho -
physiology and treatment, 2
nd edn. Saunders, Phil -
adelphia, pp 68–69.
7)
Ho
ltback U, Aperia AC (2003) Molecular deter
- minant
s of sodium and water balance during
ea
rly
human development. Semin Neonatol 8: 291–299.
8)
Wa
dei HM, Textor SC (2012) The role of the kidney
in regulating arterial blood pressure. Nat Rev Ne -
phrol 8: 602–609.
9)
Ro
cchini AP, Key J, Bondie D, Chico R, Moorehead
C, Katch V, Martin M (1989) The ef fect of weight
loss on the sensitivity of blood pressure to sodi -
um in obese adolescents. N Engl J Med 321:
580–585.
10)
Fr
isoli TM, Schmieder RE, Grodzicki T, Messerli FH
(2011)
Be
yond
sa
lt:
li
festyle
mo
difications
an
d
bl
ood pressure. Eur Heart J 32: 3081–3087.
11)
Kh
undmiri SJ (2014) Advances in understanding
the role of cardioglycosides in renal control of
salt homeostasis. J Endocrinol. doi: 10.1530/JOE-
13 – 0613.
12)
Si
monetti GD, Mohaupt MG, Bianchetti MG (2012)
Monogenic forms of hypertension. Eur J Pediatr
171: 14 33–14 39.
13)
Me
neton P, Jeunemaitre X, de Wardener HE, Mac -
Gregor GA (2005) Links between dietar y salt in -
take, renal salt handling, blood pressure, and
cardiovascular diseases. Physiol Rev 85: 679–715.
14)
Ti
tze J (2014) Sodium balance is not just a renal
af fair. Curr Opin Nephrol Hypertens 23: 101–105.
15)
Ma
r var PJ, Gordon FJ, Harrison DG (2009) Blood
pressure control: salt gets under your skin. Nat
Med 15: 487–488.
16)
Gu
ignard JP (1982) Renal function in the newborn
infant. Pediatr Clin N Am 29: 777–790.
17)
He
rin P, Aperia A (1994) Neonatal kidney, fluids, and
electrolytes. Curr Opin Pediatr 6: 154–157.
1Prof. ffRPofTff.aTb
1Prof. PRTaPR. Rbi
27
18) Gattineni J, Baum M (2013) Developmental changes
in renal tubular transport-an overview. Pediatr
Nephrol. doi: 10.1007/s00467-013-2666-6.
19)
Al
- Dahhan J, Haycock GB, Nichol B, Chantler C,
Stimmler L (1984) Sodium homeostasis in term and
preterm neonates. III. Effect of salt supplementa -
tion. Arch Dis Child 59: 945–950.
20)
Ma
rrero NM, He FJ, Whincup P, MacGregor GA
(2014) Salt intake of children and adolescents in
South London: consumption levels and dietary
sources. Hypertension 63: 1026–1032.
21)
He F
J, Marrero NM, MacGregor GA (2008) Salt and
blood pressure in children and adolescents. J Hum
Hypertens 22: 4–11.
22)
Ya
ng Q, Zhang Z, Kuklina EV, Fang J, Ayala C, Hong
Y, Loustalot F, Dai S, Gunn JP, Tian N, Cogswell ME,
Merritt R (2012) Sodium intake and blood pressure
among US children and adolescents. Pediatrics
1 3 0 : 611 – 619.
23)
Br
own IJ, Tzoulaki I, Candeias V, Elliott P (2009) Salt
intakes around the world: implications for public
health. Int J Epidemiol 38: 791–813.
24)
He
FJ, MacGregor GA (2006) Importance of salt in
determining blood pressure in children: meta-
analysis of controlled trials. Hypertension 48:
861–869.
25)
Bi
rch LL, Fisher JO (1998) Development of eating
behaviors among children and adolescents. Pedia -
trics 101: 539–549.
26)
Mi
ersch A, Vogel M, Gausche R, Siekmeyer W,
Pfaf fle R, Dittrich K, Kiess W (2013) Blood pressure
tracking in children and adolescents. Pediatr Ne -
phrol 28: 2351–2359.
27)
Ma
ncia G, Fagard R, Narkiewicz K, Redon J, Zan -
chetti A, Bohm M, Christiaens T, Cifkova R, De Ba -
cker G, Dominiczak A, Galderisi M, Grobbee DE,
Jaarsma T, Kirchhof P, Kjeldsen SE, Laurent S, Ma -
nolis AJ, Nilsson PM, Ruilope LM, Schmieder RE,
Sirnes PA, Sleight P, Viigimaa M, Waeber B, Zannad
F (2013) 2013 ESH/ESC Guidelines for the manage -
ment of arterial hypertension: the Task Force for
the management of arterial hypertension of the
European Society of Hypertension (ESH) and of the
European Society of Cardiology (ESC). J Hypertens
3 1 : 1 2 8 1 –1 3 5 7.
28)
Wi
lson DKC, Coulon S (2011) Influence of dietar y
electrolytes on childhood blood pressure. In: Flynn
JT,
Ing
elfinger
JR
,
Por
tman
RJ (e
ds)
Pe
diatric
hy
per-
tension, 2
nd edn. Springer, New York, pp 259–289.
29) Sa
saki N (1979) The salt factor in apoplexy and
hypertension: epidemiological studies in Japan. In:
Yamori Y (ed) Prophylactic approach to hyperten -
sive diseases. Raven, New York, pp 467–474.
30)
Fa
lkner B, Daniels SR (2004) Summar y of the fourth
report on the diagnosis, evaluation, and treatment
of high blood pressure in children and adolescents.
Hypertension 44: 387–388.
31)
Ap
pel LJ, Moore TJ, Obarzanek E, Vollmer WM,
Svetkey LP, Sacks FM, Bray GA, Vogt TM, Cutler JA,
Windhauser MM, Lin PH, Karanja N (1997) A clinical
trial of the ef fects of dietar y patterns on blood
pressure. DASH Collaborative Research Group. N
Engl J Med 336: 1117–1124.
32)
Sa
cks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray
GA, Harsha D, Obarzanek E, Conlin PR, Miller ER
3rd, Simons - Morton DG, Karanja N, Lin PH; DASH -
Sodium Collaborative Research Group (2001) Ef -
fects on blood pressure of reduced dietar y sodium
and the Dietar y Approaches to Stop Hypertension
(DASH) diet. DASH - Sodium Collaborative Research
Group. N Engl J Med 344: 3–10.
33)
Ge
leijnse JM, Grobbee DE, Hofman A (1990) Sodium
and potassium intake and blood pressure change
in childhood. BMJ 300: 899–902.
34)
Wi
lson DK, Sica DA, Miller SB (1999) Ef fects of potas -
sium on blood pressure in salt-sensitive and salt-re -
sistant black adolescents. Hypertension 34: 181–186. 35)
He F
J, Marrero NM, MacGregor GA (2008) Salt in
-
take is related to soft drink consumption in children
and adolescents: a link to obesity? Hypertension
51: 6 2 9 – 6 3 4 .
36. Simonetti GD, Raio L, Surbek D, Nelle M, Frey FJ, Mohaupt MG (2008) Salt sensitivity of children with
low birth weight. Hypertension 52: 625–630.
37)
Wa
ng Y, Lobstein T (2006) Worldwide trends in
childhood over weight and obesity. Int J Pediatr
Obes 1: 11–25.
38)
Bu
cher BS, Ferrarini A, Weber N, Bullo M, Bianchet
-
ti MG, Simonetti GD (2013) Primar y hypertension
in childhood. Curr Hypertens Rep 15: 444–452.
39)
Fl
ynn J (2013) The changing face of pediatric hyper
-
tension in the era of the childhood obesity epide -
mic. Pediatr Nephrol 28: 1059–1066.
40)
De B
oer MP, Ijzerman RG, de Jongh RT, Eringa EC,
Stehouwer CD, Smulders YM, Serne EH (2008)
Birth weight relates to salt sensitivity of blood
pressure in healthy adults. Hypertension 51: 928–
932.
41)
Pa
lacios C, Wigertz K, Martin BR, Jackman L, Pratt
JH, Peacock M, McCabe G, Weaver CM (2004) So -
dium retention in black and white female adole -
scents in response to salt intake. J Clin Endocrinol
M et ab 89: 1858–1863.
42)
Fr
anks PW, Hanson RL, Knowler WC, Sievers ML,
Bennett PH, Looker HC (2010) Childhood obesity,
other cardiovascular risk factors, and premature
death. N Engl J Med 362: 485–493.
43)
Da
hl LK, Knudsen KD, Heine MA, Leitl GJ (1968)
Ef fects
of ch
ronic
ex
cess
sa
lt
in
gestion.
Mo
difica
-
tion of experimental hypertension in the rat by va -
riations in the diet. Circ Res 22: 11–18.
44)
Ho
fman A, Hazebroek A, Valkenburg HA (1983) A
randomized trial of sodium intake and blood pres -
sure in newborn infants. JAMA 250: 370–373.
45)
Ge
leijnse JM, Hofman A, Witteman JC, Hazebroek
A A, Valkenburg HA, Grobbee DE (1997) Longterm
ef fects of neonatal sodium restriction on blood
pressure. Hypertension 29: 913–917.
46)
Br
ion MJ, Ness AR, Davey Smith G, Emmett P, Ro
-
gers I, Whincup P, Lawlor DA (2008) Sodium intake
in
in
fancy
an
d
bl
ood
pr
essure
at 7 ye
ars:
fin
dings
fr
om the Avon Longitudinal Study of Parents and
Children. Eur J Clin Nutr 62: 1162–1169.
47)
Whit
ten CF, Stewart RA (1980) The effect of dietary
sodium in infancy on blood pressure and related
factors. Studies of infants fed salted and unsalted
diets fo
r fiv e mo nths at ei ght mo nths an d ei ght ye
ars of age. Acta Paediatr Scand Suppl 279: 1–17.
48)
Lo
pez AD, Mathers CD, Ezzati M, Jamison DT, Mur-
ray CJ (2006) Global and regional burden of disease
and risk factors, 2001: systematic analysis of po -
pulation health data. Lancet 367: 1747–1757.
49)
Gr
imes CA, Riddell LJ, Campbell KJ, Nowson CA
(2013) Dietar y salt intake, sugar-sweetened bever -
age consumption, and obesity risk. Pediatrics 131:
14 –21.
50)
Re
bholz CM, He J (2011) Urinar y sodium excretion
and cardiovascular disease mortality. JAMA
306:1083–1084, author reply 1086–1087.
51)
Co
ok NR (2011) Urinar y sodium excretion and
cardiovascular dis- ease mortality. JAMA 306:
1085, author reply 1086–1087.
52)
St
olarz-Skrzypek K, Kuznetsova T, Thijs L, Tikho-
nof f V, Seidlerova J, Richart T, Jin Y, Olszanecka A,
Malyutina S, Casiglia E, Filipovsky J, Kawecka-Jas -
zcz K, Nikitin Y, Staessen JA (2011) Fatal and non -
fatal outcomes, incidence of hypertension, and
blood pressure chang- es in relation to urinar y so -
dium excretion. JAMA 305: 1777–1785.
53)
Bo
chud M, Guessous I, Bovet P (2011) Urinar y so-
dium excretion and cardiovascular disease morta -
lity. JAMA 306: 1084, author reply 1086–1087.
Correspondance
G. D. Simonetti
Pediatric Department of Southem
Switzerland
6500 Bellinzona, Switzerland
giacomo.simonetti @ eoc.ch
No Conflict of interest.
fl
fl
Informations complémentaires
Auteurs
A. G. Sebastiano Mario G. Bianchetti Prof. Dr. med. Giacomo D. Simonetti , Istituto pediatrico della Svizzera Italiana, Ente Ospedaliero Cantonale, Bellinzona & Università della Svizzera Italiana, Lugano, Andreas Nydegger