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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