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(1)

COMMITTEE

ON

NUTRITION

CHILDHOOD

DIET AND

CORONARY

HEART

DISEASE

A

SUBCOMMITTEE of the Inter-Society

Commission for Heart Disease

Re-sources recently recommended an

immedi-ate, nationwide change in dietary habits to

reduce the risk of coronary heart disease in

later life.1 Specifically, the Commission

urges that people eat less than 300 mg of

cholesterol each day, that the total calories

from fat be less than 35% of the diet, and

that the fat calories essentially be divided

equally among saturated, monounsaturated,

and polyunsaturated sources.

(

A

commen-tary on these recommendations appears in

this issue of Piummics.2)

The Committee on Nutrition, realizing

that pediatricians will increasingly be asked

about diets for children to reduce the risk

of heart disease in later life, has evaluated

the Commission’s report for its application

to pediatric practice. The Committee

stresses that such dietarij intervention Li, at

present, experimental and recommends

against dietary changes for all children.

Di-etary intervention may be warranted in

spe-cia! circumstances, but not before 1 year of

age. Reasons for these recommendations

will be given in this report.

The evidence relating dietary cholesterol

to coronary heart disease is summarized as

follows:

1. Some inborn or acquired diseases with

hypercholesterolemia are associated with

premature atherosclerosis.

2. Serum cholesterol levels are higher

than usual in persons with coronary heart

disease.

3. Persons with high cholesterol levels in

prospective studies developed coronary

heart disease more often than those with

normal levels.

4. The mortality rate from coronary

heart disease in different countries varies in

relation to the average blood cholesterol

values

(

or dietary fat intake).

5. Experimentally induced

hypercho-lesterolemia in animals is associated with

atherosclerotic deposits.

6. Atherosclerotic plaques contain lipids

similar in composition to those in the

blood.1’3

The foregoing evidence would be more

persuasive if restriction of dietary

choles-terol in the population at large could be

shown to reduce the frequency of coronary

heart disease. To date, the results of studies

on this subject are far from convincing.4

Since a large-scale study designed to

re-solve this issue for the general population

in the United States would take at least 10

years to complete, the Commission has

urged an immediate, nationwide campaign

to reduce dietary cholesterol-with

concur-rent evaluation of the effects on the

mci-dence of coronary heart disease.1 In

addi-tion, the Commission has stressed the need

to control obesity, diabetes mellitus, and

two other major risk factors-hypertension

and cigarette smoking.

However, the foregoing are not the only

determinants of coronary heart disease.

Re-cent progress has been made in defining the

ro!e of genetics in heart disease. People

with familial type II hyperlipoproteinemia

are particularly prone to coronary heart

dis-ease. This trait, apparently transmitted as

an autosomal dominant, has been

provision-ally estimated to be present in as many as 1

in

200

newborn infants.5’ It has also been

estimated that, among male heterozygotes

with this trait, the chance of developing

is-chemic heart disease is 5% by age 30, 51%

by age 50, and 85% by age 60. This is a

tremendous morbidity rate from a single

disease. The frquencies for women with this

trait are less, although much greater than

the normal rate.6 Disability among

pre-sumed homozygotes with type II defect is

greater and occurs earlier than among

het-erozygotes. Homozygotes may have

xan-thomas and vascular disease before 10 years

of age. The other forms of familial

hyperli-poproteinemia (types I, III, IV, and V) are

rare in children.

Unproven preventive measures should be

tested first in a group at exceptionally high

risk of the disease concerned. Thus, polio

(2)

306 DIET AND CORONARY DISEASE

virus vaccine was initially administered to

children in the first three grades of primary

school because they were known to have

the highest attack rates. Similarly, dietary

intervention should, before being

recom-mended for everyone, be tested in persons

with an exceptionally high risk of having

coronary heart disease-namely, those with

familial type II hyperlipoproteinemia.6

Identifying these individuals early in life is

feasible, and motivation for dietary

restric-lions is likely to be greater in affected

fami-lies than in the general population. The

benefits, or possible adverse effects, of

di-etary changes can be evaluated from a

study of this special group before changes

are recommended for the population at

large. A nationwide alteration in diet may

well impair the sense of well-being of the

general public, apart from any unforeseen,

organic harm.

The modified diet for persons with

famil-ial type II defect may not provide a

con-vincing answer to the benefits to be derived

by the population at large; however, it will

provide some experience as to safety,

ac-ceptability, and effectiveness of the general

approach. Until the results of such trials are

available, the Committee does not support

the CommLcsion’s recommendation for

di-etary intervention for all children.

How-ever, pediatricians should identify children

with familial type II defect and recommend

the appropriate diet for them.

A family history of coronary heart disease

before 50 years of age in first cousins or

closer relatives justifies obtaining a fasting

serum specimen from the child for

choles-terol, triglyceride, and lipoprotein analysis.

Such determinations cannot as yet be

rec-ommended before 1 year of age because

normal values during infancy are only now

in the process of being established. Other

family members should be studied when a

lesterol for children from 1 to 12 years of

age with type II hyperlipoproteinemia

should be kept as low as possible. A

hand-book concerning the disease and the diet

can be obtained from the National Heart

and Lung Institute8 or the American Heart

Association. The diet for type II

hyperlipo-proteinemia is considered to be therapeutic

and is not designed for the general

popula-tion or for patients with other forms of

hy-penlipoproteinemia.

A sustained reduction of at least 10% in

serum cholesterol or triglyceride levels

sig-nifies that a dietary effect has been

achieved, and the diet should be continued.

At present, there is no good reason for

ini-tiating the diet before 1 year of age,

espe-cially since the benefits from present infant

feedings are too great to be jeopardized.

When the diet is begun, care must be

taken, of course, to insure that food

constit-uents essential to normal growth are

pro-vided in adequate quantities. Drugs to

control type II hyperlipoproteinemia in

chil-dren should only be used if the condition is

severe and does not respond to dietary

ther-apy alone.

Families with no evidence of type II

hy-perlipoproteinemia who request guidance

about diets to reduce coronary heart

dis-ease can be advised that no harm is known

to occur from moderate dietary alteration

and, conceivably, that some benefits may

accrue. In particular, this may apply to

children with diabetes mellitus or a strong

family history of diabetes, as well as to

chil-dren in families having a history of early

coronary heart disease not related to type II

defect; in these instances, no therapeutic

regimen would be prescribed. For these

children, the diet proposed by the

Inter-So-ciety Commission for Heart Disease

Re-sources’ would be appropriate : adjust

(3)

AMERICAN ACADEMY OF PEDIATRICS 307

COMMIrrEE ON Nu’rnrnoN

L.

J.

Fiun, JR., M.D., Chairman

LEWIS A. BARNES5, M.D.

Riciziin B. GOLDBLOOM, M.D.

J

AMES C. HAWORTH, M.D.

MALCOLM A. HOLLIDAY, M.D.

ROBERT W. Miuini, M.D.

DONOUGH O’BiuiN, M.D.

Howuw A. PEisoN, M.D.

CHARLES R. ScRIVER, M.D.

WILLIAM B. WElL,

Ju.,

M.D.

CHARLES F. WHITFEN, M.D.

J

OAQUIN CRAVIOTO, M.D.

(

Consultant) 0. L. KLINE, PH.D.

(

Consultant)

REFERENCES

1. Report of Inter-Society Commission for Heart

Disease Resources : Primary prevention of the atherosclerotic diseases. Circulation, 42, No. 6: A-55, 1970.

2. Mitchell, S., Blount, S. C., Blumenthal, S.,

Jesse, M. J., and Weidman, W. H. : The

pedi-atrician and atherosclerosis. PEDIATRICS, 49:

165, 1972.

3. Kannel, W. B., Castelli, W. P., Gordon, T., and McNamara, P. M. : Serum cholesterol, lipopro-teins and the risk of coronary heart disease. Ann. Intern. Med., 74:1, 1971.

4. Cornfield, J., and Mitchell, S.: Selected risk fac-tons in coronary disease : Possible intervention effects. Arch. Environ. Health, 19:382, 1969.

5. Glueck, C. J., Heckman, F., Schoenfeld, M.,

Steiner, P., and Pearce, W. : Neonatal familial

type II hyperlipoproteinemia: Cord blood

cholesterol in 1,800 births. Metabolism, 20:

597, 1971.

6. Fredrickson, D. S.: Mutants, hyperlipoprotein-aemia, and coronary artery disease. Brit. Med. J., 2:187, 1971.

7. Slack, J.: Risks of ischaemic heart disease in familial hyperlipoproteinaemic states. Lancet, 2:1380, 1969.

8. Dietary Management of Hypenlipoproteinemia.

A Handbook for Physicians. Pp. 14-23,

1970. Available free from the Office of Heart

and Lung Information, Building 31, Room

(4)

1972;49;305

Pediatrics

William B. Weil, Jr., Charles F. Whitten, Joaquin Cravioto and O. L. Kline

Holliday, Robert W. Miller, Donough O'Brien, Howard A. Pearson, Charles R. Scriver,

L. J. Filler, Jr., Lewis A. Barness, Richard B. Goldbloom, James C. Haworth, Malcolm A.

CHILDHOOD DIET AND CORONARY HEART DISEASE

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(5)

1972;49;305

Pediatrics

William B. Weil, Jr., Charles F. Whitten, Joaquin Cravioto and O. L. Kline

Holliday, Robert W. Miller, Donough O'Brien, Howard A. Pearson, Charles R. Scriver,

L. J. Filler, Jr., Lewis A. Barness, Richard B. Goldbloom, James C. Haworth, Malcolm A.

CHILDHOOD DIET AND CORONARY HEART DISEASE

http://pediatrics.aappublications.org/content/49/2/305

the World Wide Web at:

The online version of this article, along with updated information and services, is located on

American Academy of Pediatrics. All rights reserved. Print ISSN: 1073-0397.

References

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