AMERICAN ACADEMY OF PEDIATRICS · Love5 as one factor, and they have recom-mended that dietary salt...
Transcript of AMERICAN ACADEMY OF PEDIATRICS · Love5 as one factor, and they have recom-mended that dietary salt...
AMERICAN ACADEMY OF PEDIATRICS
115
COMMITTEE ON NUTRITION
SALT INTAKE AND EATING PATTERNS OF INFANTS AND
CHILDREN IN RELATION TO BLOOD PRESSURE
Essential hypertension is a major health
problem in the adult population in the
United States; and its association with heart
disease, stroke, and renal failure ( particu-
larly among patients in the third and fourth
decades ) has made efforts for its preven-
tion a matter of high priority.1 Twenty
percent of the adult population has hy-
pertension or hypertensive heart disease.1
Multiple factors24 contribute to the devel-
opment of hypertension. The level of di-
etary salt intake by persons in the United
States has been proposed by Dahl and
Love5 as one factor, and they have recom-
mended that dietary salt intake by persons
in this country be lowered.
Dahl6 has suggested that the salt intake
of infants and children predisposes to hy-
pertension later in life, and he has focused
on the salt content of processed infant
foods. This is of concern because dietary
intake of salt by infants sometimes exceeds
minimum requirements by four to six
times,7 and because salt feeding early in
life in hypertensive-sensitive rats8 has in-
duced hypertension more readily than
when salt is provided later.
A subcommittee of the Food ProtectionCommittee of the Food and Nutrition
Board ( NAS-NRC) reviewed the subject#{176}
and concluded that, whereas average salt
intake of infants was indeed several times
the minimum requirement, evidence relat-
ing salt intake to hypertension later in life
was ambiguous. The committee recom-
mended that the salt content of infant foods
be reduced. Manufacturers have complied,
and subsequent surveys10 have shown a
reduction in salt intake of infants less than
8 months old. However, the salt intake of
older infants remains unchanged, and chil-
dren of all ages appear to have a salt intake
well in excess of the estimated minimum
requirements. The salt intake of infants and
children and its possible relation to hyper-
tension continue to lead to recommenda-
tions that dietary salt intake should be
decreased.”
Difficulties arise in attempting to recom-
mend a suitable range for dietary salt be-
cause of the tremendous range of biological
tolerance in normal human beings, the
widely different levels of salt appetite, and
the cultural significance which salt has in re-
lation to food.’2 The Committee on Nutri-
tion has reviewed the factors which affect
dietary salt intake, including changes in
cultural patterns that may alter the quan-
tity of salt ingested. The Committee has
also reviewed current thinking on the
causes of hypertension and the evidence
relating salt intake to hypertension. The
Committee recommends actions that reduceor avoid increasing the present level of salt
intake by children in the population at
large. Children with a family history of
hypertension may benefit from a low salt
diet, although the evidence to date is
incomplete.
SALT TOLERANCE AND DIETARY PATTERNS
Dietary Salt Intake of Adults
The human adult who is not subjected to
unusual salt losses from sweating or losses
of gastrointestinal or other body fluids can
maintain health and normal activity on
little sodium (Na).#{176} Certain societies ex-
ist for whom virtually no sodium is avail-
able.1’ Kempner1’ demonstrated that pa-
tients with hypertension could sustain nor-
ma! activities for months on diets containing
as little as 2 mEq of Na per day. Hence,
0 Salt is used in the paper to refer to sodium
chloride; Na refers to the sodium content of thediet. Where Na content is high, the chloride con-
tent also is high in nearly every instance.
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116 HYPERTENSION
TABLE I
NA INTAKE OF INFANTS AT 6 MONTHS OF AGE
Total
mEq/day
Dietary Salt Intake
,Va:K
/kg /lOOkcal
Infant-human milk 6-8 1 1.0 0.6Puyau average7 45 ± 12 6 6 0.7-1.5
6-month-old infant
10
1969 survey 40-45 6 6 1.15
1972 survey 25-30 3-4 3-4 0.89
Adult 150-200 2-3 6-8 1.2-2.0
Note: Detailed data from Purvis et at. kindly provided to the Committee.
the minimum requirement ( 0.1 mEq/100
kcal ) for normal adults in a favorable
setting is low; it is higher for those experi-
encing skin losses from sweating and for
pregnant and lactating women. The maxi-
mum tolerance for adults is high. Japanese
and Thai farmers ingest 20 to 25 gm of salt,
400 to 500 mEq of Na per day (20 mEq/ 100
kcal), with no signs of salt toxicity, i.e.,
edema or hypernatremia.3 A few individ-
uals are reported to ingest 1,000 mEq of Na
per day habitually without evident harm.The capacity to adapt to a low intake
may derive from man’s evolutionary roots
as an herbivorel2; the biological advantages
of his tolerance to a high intake are less
clear. Access to a high intake provides re-
placement when salt is lost from the body
as sweat or gastrointestinal losses. Histori-
cally, salt was a valued preservative, par-
ticularly for meat and fish. Other mammals,
notably herbivores, seek salt from salt licks
but probably do not ingest salt in quantities
comparable to modern man. The search for
salt derives from an appetite for salt which
is stimulated by salt deficiency, notably
in herbivores. However, an appetite for
salt can be acquired as an individual
2
The ability of humans to adapt to a wide
range of sodium intake is due to the renal-
endocrine system responsible for regulating
body sodium, within narrow limits, by
varying urinary excretion of sodium ac-
cording to sodium intake and nonrenal so-
dium losses. The hormonal system ( renin,
angiotensin, and adrenal mineralocorti-
coids ) � and the kidney’5 are key factors in
the physiological regulation of blood pres-
sure; and there is evidence for considerable
genetically determined variability within
this control system. Also, regulation of
body potassium (K ) in response to varia-
tion in intake of K is dependent on ele-
ments in the sodium control system. Blood
pressure is affected by variations in the
ratio of Na :K in diet as well as the dietary
Na alone.
Food patterns often have changed as a
result of the vagaries of history, but they
stabilized where food sources became de-
pendable and cultural patterns became set.
In the last 100 years, food sources in the
United States have undergone vast change
and the process continues. The major ele-
ment of this change in our society has been
linked to the movement of people from a
rural setting to cities and suburbs. Coinci-
dentally, established cultural ties often
have been disrupted and food sources have
changed, with increasing dependence on
processed or manufactured foods as the
principal food source.
There is some evidence from marketing
data that average per capita adult salt con-
sumption has not changed in the last few
decades, despite the change in food
sources; presently, the average per capita
consumption of Na per day is 150 to 200
mEq.16 However, the proportion of Na
provided from consumer purchase of salt
has declined, and that provided from pro-
cessed or prepared foods has increased.’7
Salt intake has become increasingly deter-
mined by food processors, rather than by
individuals.
Salt Intake of Infants
The minimum salt requirement for the
infant actually exceeds that of the adult.
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AMERICAN ACADEMY OF PEDIATRICS 117
TABLE II
SOURCE OF SALT IN THE U.S. INFANT’S Di�T-1972 SURVEY OF 374 INFANTS
Age (mo)
mEq ofXape r Day
2 4 6 8 10 12
From
Formula 8.0 4.5 1.5 1.0 1.0 0
Milk 2.0 7.0 12.5 13.5 12.5 12Babyfood 3.5 7.5 12.0 15.0 13.5 12Tablefood5 0 0 3.0 9.5 24.0 39
Total 13.5 19.0 29.0 38.0 51.0 63
Estimated sodium of
of an infant re-
ceiving only human
milk 6 7 8 9 10 12
* Sodium content estimated from Handbook #8, U.S. Department of Agriculture, December 1963. Does
not include table salt.
One to two mEq of Na per day is required
for growth; skin and gastrointestinal losses
for children are estimated to be 2 mEq/ day.
These plus obligatory urinary losses result
in a requirement of 6 to 8 mEq of Na per
day.18”9 Growth rate, stool composition, and
skin losses are more important determinants
of the daily salt requirement than body size
or caloric need during the first year of life.
The traditional source of sodium for the
infant has been human milk, which pro-
vides 5 to 10 mEq of Na per day ( 1 mEq/
100 kcal) ; infants receiving human milk of-
ten excrete less than 2 mEq of Na per day.
The Na:K ratio of human milk (and most
mammalian milk) is 0.6 to 0.7 mEq. The
potassium requirement for growth exceeds
the sodium requirement.Renal mechanisms for conserving and
excreting salt are well developed in the
infant from 1 month of age. However,
extrarenal losses, such as occur in gastro-
enteritis, are more likely to lead to salt
depletion or hyponatremia in infants than inadults. Conversely, the infant with re-
stricted access to water is at greater risk
of salt excess and hypematremia.
Infants, as is true with adults, have a
tolerance for a salt intake several times the
minimum. Intakes of 100 mEq of Na per day
(10 mEq/100 kcal) without adverse effects
are observed.7 While higher intakes may
be possible, the phenomenon of hyperna-
tremia is a greater risk to infants because
their access to water may be limited, and
higher salt intakes require higher water in-
gestion for effective renal regulation.
Hence, the safe tolerance limits for childrenappear to be roughly between 8 and 100
mEq of Na per day. While this range is con-
siderable it is less than that of the adult. Ex-
cept for a few uncommon adrenal disorders,
the lower intakes of sodium recommended
for infants are compatible with maintenance
of normal potassium balances within the
range of any normal, dietary intake.
In the past 50 years, the pattern of salt
intake among infants has undergonechange. Through the first 6 to 9 months of
life, infants in the United States used to
be fed human milk as the principal source
of nutrients; and up until the turn of the
century, they received from 5 to 10 mEq ofNa per day. A trend to adopt modified cows’
milk in place of human milk began in the
early 1900s and resulted in a two- to three-
fold increase in sodium intake and a pro-
portional increase in potassium. The intro-
duction of solid food into the young infant’s
diet also became more popular; as a result,the salt intake increased in varying degrees.Presalted cereals, meats, and vegetables
contributed to the sodium intake; fruit didnot. The salt was added to the diet either
in home or commercial preparations to
satisfy the mother’s salt appetite. Because
infants accept salted and unsalted food in
equal amounts,2#{176} the salt content of the
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118 HYPERTENSION
food has little effect on its consumption;
and, it probably reflects the mother’s cul-
turally acquired appetite for salt.
Puyau and Hampton,7 who reported the
daily Na intake of infants during the first
year of life in 1960, found a considerable
variation; but the mean intake increased
from 30 mEq/day at 2 to 3 months to 45
mEq at 6 to 8 months and to 60 mEq at
11 to 13 months. Table I compares salt
intake of infants at 6 months of age taken
from their diet survey7 with the results of
surveys done in 1969 and 1972,’#{176}and with
the intake of a breast-fed, 6-month-old in-
fant and an average adult. The average
intakes exceed those provided from human
milk by four- to sixfold; the maximum in-
take was 100 mEq of Na per day. The lower
Na intake in the 1972 survey reflects manu-
facturing changes in 1970, when salt content
was reduced. Salt intake of infants com-
pared with adults is higher per kilogram of
body weight, but lower in relation to caloric
intake. The Na:K ratios are comparable.
Sodium intakes for infants 2 to 12 months
of age and the principal food sources from
which they are derived are shown in Table
II. Dairy milk and table foods increase as
principal sources of salt after 8 months of
age. Consequently, the impact of any re-
duction in salt content of infant foods
diminishes as the child passes this age.
Salt Intake of Children
Beyond infancy, when milk customarily
ceases to be the major food, children tra-
ditionally eat what their parents do. Hence,
salt intake increases with increased intake
of family food as the child grows. Family
salt intake may be determined by the fam-
ily’s cultural background, and the dietary
Na : K ratio of the child reflects his family’s.
Generally, the Na : K ratio has not ex-
ceeded 2.0.21
Margaret Mead22 has pointed out that
children no longer learn their modes of
behavior from their parents, but rather
copy the behavior of their peers or learn
from models outside the home, e.g., school,
vocation, and chosen adult models. This
trend is noticeable in relation to eating
patterns. Eating patterns for today’s school
children and adolescents increasingly are
set by fads, by commercial advertising, and
by teen-age life styles. The resulting food
consumption pattern may consist of school
lunches (which in one study2’ contained 15
mEq of Na per 100 kcal), quick-service food
suppliers, etc. One possible consequence
of this development is the tendency for
salt intake to be consistently high in all
children. Peer group pressures and uniform
food sources may make it difficult for a
child who desires it to adopt a diet low
in salt.
SALT INTAKE AND THE CAUSES
OF HYPERTENSION
Because of the prevalence of essential
hypertension in adults, there is a major
public health concern with its causes; the
reviews already cited24 outline a number
of predisposing factors. These factors in-
dude race, family history, stress, variations
in endocrine and kidney function, and
body habitus. Salt has also been cited as
causing hypertension. There is no question
that an increase in salt intake by most
hypertensive patients will increase their
blood pressure. The converse also is true.
The question is whether salt intake induces
hypertension and, in particular, whether
salt consumption by the general population
in this country is a risk.
The evidence that salt intake induces
hypertension is based on experimental
studies in rats and epidemiological studies
in humans.
Evidence in Rats Relating Hypertension to
Salt Intake
Hypertension in animals produced by
almost any experimental technique was
increased when the salt intake was in-
creased.’6
An increase in the salt content of the diet
can cause hypertension in rats. Meneely
and Ball2’ summarized their observations
of blood pressure and other responses to
the dietary manipulation of sodium, chlor-
ide, and potassium. There were no differ-
ences in growth (length and weight),
longevity, or blood pressure among animals
of 100-gm body weight fed between 0.15%
and 2.0% salt in their dry rations (0.5 =
7.0 mEq/100 kcal diet). Those fed 2.8% or
5.6% salt ( 10 or 20 mEq of Na per 100 kcal)
developed moderate hypertension, grew
slightly less, and had a shorter life-span;
when fed 7% or more salt, more severe
hypertension and growth retardation re-
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AMERICAN ACADEMY OF PEDIATRICS 119
sulted, and they had a much shorter life-
span. There was cardiac and renal enlarge-
ment proportional to the blood pressure
elevation; microscopically, arteriolar lesions
were seen, particularly in the kidney of the
severely hypertensive rats. Potassium chlo-
ride lessened the effects of high NaC1
feeding on blood pressure and life-span.
Dah124 demonstrated that feeding 8% or
more ( 25 to 30 mEq/100 kcal) salt to rats
in dry rations could result in irreversible
hypertension, but with considerable varia-
tion in blood pressure response within the
general population. He then developed a
salt-resistant and a salt-sensitive strain of
rats. A salt intake in the salt-sensitive rats
of from 0.4% to 11% of the diet correlated
with progressive elevation of blood pres-
sure.” When rats of this strain were fed
8% salt from weaning to 6 weeks of age,
they developed hypertension by 1 year of
age and their life-span was shortened.8 The
effect, both in blood pressure and life-span,
was less when the extra salt intake was pro-
vided between 3 and 6 months of age.
In summary: intakes of 10 to 30 mEq of
Na per 100 kcal/day (3 to 8 mEq/kg/day)
induce hypertension is nonselected labora-
tory rats; lesser amounts induce hyperten-
sion in genetically selected rats. Early feed-
ing of salt to sensitive rats predisposes to
hypertension later. Adding potassium to
the diet to maintain a Na:K ratio < 2.0
protects against the induction of hyper-
tension. Resistant rats tolerate high Na
intakes.
Epidemiological Studies in Humans
Dahl’6 demonstrated that some cultures
show a positive linear relation between
average salt intake and the overall preva-
lence of hypertension. Eskimos, who in-
gest an average of 30 mEq of Na per day, are
virtually free of hypertension; some Jap-
anese farmers ingest an average of 500
mEq of Na per day, and 40% of them over
40 years old are hypertensive. Average salt
consumption in the United States is 150
to 200 mEq of Na per day, and there is a
20% prevalence of hypertension among
adults over 40 years of age.
Additional studies26 have confirmed
Dahl’s findings. When blood pressure and
salt intake of two Polynesian groups were
compared,’7 the prevalence of hypertension
was greater with increasing age in the
group averaging an intake of 120 to 140
mEq of Na per day than in the group aver-
aging 60 mEq of Na per day. Disparities
have also been observed. For example, the
native population in St. Kitt’s Island in the
West Indies28 ingests 100 to 150 mEq of Na
per day and shows a much higher preval-
ence of hypertension than that occurring in
the United States.
Individuals within a culture (population)
show only negligible correlation between a
single, measured blood pressure and daily
salt intake. Dahl’6 first reported higher
blood pressures in laboratory workers who
regularly added salt to prepared food com-
pared to blood pressures in workers adding
little or no salt to prepared food. Mia1129
assessed salt intake by diet history and
urine sodium excretion and found no cor-
relation in males in a Welsh mining com-
munity and a negative correlation in
females. Prior27 also noted no correlation
between individual blood pressures and
salt intake in his “high-sale’ Polynesian
group. Dawber and his colleagues3#{176} failed
to find correlation in the “Framingham
Study” between blood pressure and daily
salt intake.
In other studies, no differences � saltexcretion were observed between hyper-
tensive and normal ti332
Dahl’6 expressed the view that salt in-
take is one of the multiple factors which
act in various degrees to cause hyperten-
sion. However, if a low salt diet diminishes
the risk of developing hypertension and a
high salt diet increases the risk, some degree
of correlation should be expected between
an individuars salt intake and his blood
pressure. Little correlation has been found.
An important limitation to all the data is the
method used to access salt ingestion over
the years, i.e., one- or two-day samples of
dietary intake by history or sodium excre-
tion in a 24-hour urine sample. A second
limitation is the relatively small sample size.
In summary: epidemiological observa-
tions suggest a relation between salt inges-
tion and hypertension but fail to support
the hypothesis that salt consumption is a
ma/or factor in causing hypertension in
persons in the United States.
SUMMARY
Approximately 20% of children in this
country are at risk of developing hyper- by guest on November 14, 2020www.aappublications.org/newsDownloaded from
120 HYPERTENSION
10. Purvis, C., Wallace, R., Harper, J. W., Lovasz,
tension as adults. The factors that will in-
duce hypertension are genetic, which can-
not be modified, and environmental, which
can be modified. Genetic factors assist in
identifying the population at risk, i.e.,
family history of hypertension, myocardial
infarction, stroke, or renal disease. The
population with a negative family history
is less at risk.
The role of salt intake as an environ-
mental factor in the induction of hyperten-
sion has still to be defined. For 80% of the
population in this country, present salt
intake has not been demonstrated to be
harmful, i.e., hypertension has not devel-
oped. Salt intake is likely to be only one
of the contributing factors for those whose
genetic makeup predisposes them to hyper-
tension.
Salt appetite for some is an important
expression of personal preference in rela-
tion to diet; for others, salt-containing foods
have important cultural values. Present
evidence does not provide a firm basis for
advising a change in the dietary salt intake
for the general population. There is a rea-
sonable possibility that a low salt intake
begun early in life may protect, to some
extent, persons at risk from developing
hypertension.
Salt consumption today is being deter-
mined to an increasing degree by food
manufacturers and processors and quick-
service food suppliers. To the extent that
salt is added to a food prior to its being
served, the individual has an obligatory
rather than a selected intake of salt. The
consumption of presalted foods may be
producing significant changes in salt in-
take which are not perceived at this time.
RECOMMENDATIONS
The Committee favors development of
guidelines for restraining the use of salt by
food processors.
As a public health measure, consumers
need more information on the salt content
of their diet. The Committee believes that
information on the amount of salt added
to processed foods should be made avail-
able to consumers.
The Committee recommends the market-
ing of foods for low salt diets ( <40 mEq of
Na per day, i.e., 1,000 mg Na diet) to make
them available at the same cost and con-
venience as diets which provide more salt.
The Committee recommends that nutri-
tion education be directed to increasing
public awareness of the potentials for di-
etary variation that can enhance the cul-
tural and social value of eating and still
conform to good nutrition practices. The
genetic and cultural heterogeneity of the
population in this country justifies a flex-
ible policy with respect to diet recommen-
dations. Salt is but one example of a
nutrient that can be enjoyed by many, but
must be restricted in some. Dietary modifi-
cation for persons at risk, rather than for the
population at large, is consistent with sound
medical and epidemiological practices.
COMMITrEE ON NuTiwrloN
MALCOLM A. HOLLIDAY, M.D., Chairman
AnNou S. ANDERSON, M.D.
LEwIs A. BARNES5, M.D.
RICHARD B. GOLDBLOOM, M.D.
JAMES C. HAWORTH, M.D.
ALVIN M. MAUER, M.D.
ROBERT W. MILLER, M.D.
DONOUGH O’BRIEN, M.D.
WILLIAM B. WElL, JR., M.D.
CHARLES F. WHITrEN, M.D.
Consultants:
J OAQUIN Ci�woTo, M.D.
L. J. FILER, JR., M.D.
0. L. Ku�, Pi�.D.ROBERT W. WINTERS, M.D.
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