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Full Chapter Pediatric Nutrition 8Th Edition Ronald E Kleinman PDF
Full Chapter Pediatric Nutrition 8Th Edition Ronald E Kleinman PDF
Kleinman
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Am P
Pediatric
er olic
Pediatric Nutrition
of ica y o
Pe n A f th
di ca e
at d
ric em
Nutrition
s y
Pediatric
Nutrition
8th Edition
Significantly revised and updated by more than 100 contributors, the eighth 8th Edition
edition provides the latest evidence-based guidance on the full spectrum of
childhood nutrition issues.
More than 50 chapters cover the latest information on nutrient metabolism
to support the normal development and health of infants and children who are
well, those born with congenital anomalies or disorders of metabolism, and
those with acute and chronic illnesses.
Tables and figures in the chapters and appendixes are designed to provide
a ready resource for a wide variety of topics that affect practice, including the
nutrient content of selected foods, recommended daily nutrient requirements,
the fortification and use of specialized infant formulas, and updated growth
charts for preterm infants after birth, including body mass index.
New in the Eighth Edition
●● New chapter: Pediatric Global Nutrition.
●● Other chapters have been completely reorganized, based on new information
in nutritional science and new evidence-based guidelines recommending
changes in practice.
●● New policy statement on sugary drinks and new clinical reports on food
8th Edition
insecurity, fruit juice consumption, and use of donor human milk for the
preterm infant.
For other pediatric resources, visit the American Academy of Pediatrics at
shop.aap.org.
AAP
Suggested Citation:
American Academy of Pediatrics
Committee on Nutrition.
[chapter title]. In: Kleinman RE,
Greer FR, eds. Pediatric Nutrition.
8th ed. Itasca, IL:
American Academy of Pediatrics;
2019:[page numbers]
The book has been developed by the American Academy of Pediatrics. The authors, editors, and
contributors are expert authorities in the field of pediatrics. No commercial involvement of any
kind has been solicited or accepted in the development of the content of this publication.
Products are mentioned for informational purposes only. Inclusion in the publication does not
imply endorsement by the American Academy of Pediatrics.
The publishers have made every effort to trace the copyright holders for borrowed material. If
they have inadvertently overlooked any, they will be pleased to make the necessary arrange-
ments at first opportunity.
Copyright © 2020 American Academy of Pediatrics. All rights reserved. No part of this publica-
tion may be reproduced, stored in a retrieval system, or transmitted in any form or by any
means, electronic, mechanical, photocopying, recording, or otherwise, without prior permis-
sion from the publisher. Printed in the United States of America.
3-337/1019
1 2 3 4 5 6 7 8 9 10
Liaison Representatives
Andrew Bremer, MD, PhD, FAAP, National Institutes of Health
Andrea Lotze, MD, FAAP, US Food and Drug Administration
Cria G. Perrine, PhD, Centers for Disease Control and Prevention
Catherine M. Pound, MD, Canadian Paediatric Society
Valery Soto, MS, RD, LD, US Department of Food and Agriculture
AAP Staff
Debra L. Burrowes, MHA
Madeline Curtis, JD
Tamar Magarik Haro
Katherine Matlin, MPP
iii
Ronald E. Kleinman, MD, FAAP, and Frank R. Greer, MD, FAAP, Editors
vii
I NUTRIENT-GENE INTERACTIONS
1. Nutrition for the 21st Century—Integrating Nutrigenetics, Nutrigenomics,
and Microbiomics. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
ix
APPENDICES
A Components of Human Milk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1503
B Infant Formula Act Regulations and Expert
Recommendations for Term US Infant Formulas. . . . . . . . . . . . . . . . . . . . . . . . 1517
C Increasing Caloric Density of Infant Formula. . . . . . . . . . . . . . . . . . . . . . . 1519
D D-1: Formulas for Low Birth Weight and Preterm Infants. . . . . . . . . . . . . . 1521
D-2: Human Milk Fortifiers for Infants Fed Human Milk. . . . . . . . . . . . . . 1526
E E-1: DRI Recommended Intakes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1531
E-2: DRI Tolerable Upper Intakes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1536
F ChooseMyPlate. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1541
G Food-Drug Interactions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1549
H Calories and Electrolytes in Beverages . . . . . . . . . . . . . . . . . . . . . . . . . . 1563
I Dietary Fiber: Food Sources Ranked by Amounts of Dietary Fiber and
Energy per Standard Food Portions and per 100 Grams of Foods. . . . . . . . . . 1567
J Calcium Contents of Common Foods. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1571
K Iron Content of Selected Foods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1575
L Zinc Content of Common Foods. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1577
M M-1: Selected Enteral Products for Special Indications. . . . . . . . . . . . . . . . 1579
M-2: Enteral Products Grouped by Usage Indication . . . . . . . . . . . . . . . . 1604
M-3: Medical Food Modules and Modified Low Protein Foods for
Treatment of Inborn Errors of Metabolism. . . . . . . . . . . . . . . . . . . . . . . . . . . 1606
N Sports/Nutrition Bars. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1611
O Sodium Content of Foods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
P Saturated and Polyunsaturated Fat and Cholesterol
Content of Common Foods. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1617
Q Growth Charts. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1623
Introduction
The importance of nutrition influences on human health and disease at the
genetic and molecular levels are becoming increasingly clear. Interactions
between diet and the genome can affect health and disease via many
interconnected pathways including RNA expression (the transcriptome),
epigenetics modification (the epigenome), intermediary metabolites (the
metabolome including the lipidome and the proteome), and resident micro-
biological communities in the gastrointestinal tract—the microbiome1 (see
Fig 1.1). Some may even include among these interconnective pathways the
so called “inflammasome,” beyond the scope of this chapter, which consists
of the functional responses receptors and sensors that regulate the activa-
tion of the innate immune system in response to infectious microbes and
molecules derived from host proteins.2 Current information and recom-
mendations are largely based on epidemiologic studies of populations in the
absence of specific knowledge of the individual’s genetics and the individual
metabolic response to nutrients, which may result in erroneous nutritional
recommendations. One example is the concept “milk, it does the body
good,” which applies appropriately to all the population during infancy but
to half or less of the world’s population after infancy and early childhood,
when symptoms of lactose intolerance may preclude ingesting dairy prod-
ucts in significant quantities.
Before the sequencing of genomes was completed, the research com-
munity was unable to take an integrative approach to explore the role of the
diet in disease and well-being. Most experimental designs (including epide-
miologic studies) used common, well characterized, but relatively uninfor-
mative biomarkers to advance understanding of various disease states. For
example, studies aimed at elucidating the molecular mechanisms promot-
ing cardiovascular diseases have primarily used classical biomarkers, such
as plasma cholesterol, triglycerides, or C-reactive protein, rather than ones
that provide a more accurate and highly predictable assessment of an indi-
vidual’s response to a nutrient or diet over time. The traditional paradigm
has been based on epidemiologic and interventional studies, which did not
include family history and environmental exposure. This focus resulted in
dietary recommendations using the MyPyramid or MyPlate approach for an
entire population rather than an ‘n=1’ (one’s self) approach.3
Fig 1.1.
The environment and the diet interact via nutrigenetics with the human
genome and its closely related epigenome and microbiome to influence
health and disease via nutrigenomics effects.
Environment
Diet/Nutrients
Nutrigenetics
Human Genome
• Transcriptome
• Metabolome
Epigenome Microbiome
· proteome
· lipidome
• Inflammasome
Nutrigenomics
Nutrigenetics
Human beings are not genetically identical and live in different environ-
ments. Thus, each person’s response to diet would not be expected to be
equivalent. Nutrigenetics refers to gene-nutrient interactions and how an
individual responds to a certain diet on the basis of one’s genome and, thus,
considers many underlying genetic polymorphisms.4
The following are examples of gene-nutrient interactions:
1. For decades, dietary interventions have been required of individuals
with phenylketonuria or galactosemia. These “inborn errors of me-
tabolism” are caused by a single-gene defect that responds to dietary
treatment with a low-phenylalanine or low-galactose diet. Phenylketon-
uria is characterized by the defective phenylalanine hydroxylase (PAH)
enzyme, resulting in the accumulation of phenylalanine in the blood,
which drastically increases the risk of neurologic damage. Galactose-
mia is caused by a rare recessive trait in galactose-1-phosphate uridyl
transferase (GALT), leading to the accumulation of galactose in the
blood and increasing the risk of mental retardation. Galactose-free or
phenylalanine-restricted tyrosine-supplemented diets are a means to
treat these monogenic diseases nutritionally.
2. Individuals with certain mutations in the enzyme 5,10-methylene
tetrahydrofolate reductase (MHTFR) respond idiosyncratically to folate
if they consume the recommended intakes of folate established by
the dietary guidelines. A specific thermolabile variant of this enzyme,
which elevates blood homocysteine levels, has been described in 5% to
15% of the population. This variant is associated with a hypercoagulable
state and an increased risk of pregnancy loss and birth defects. Using
red cell and plasma folate concentrations, it has been found that folate
concentrations are low in nonpregnant women and even lower in preg-
nant women with a homozygous variant of this gene.5 Dietary interven-
tion with methlyfolate supplementation requires closer observation of
pregnant women with this variant.
3. Intestinal fatty acid binding protein (IFABP) is exclusively expressed in
the small intestine. IFABP is believed to bind and transport long-chain
fatty acids (LCFAs) in the cytoplasm of columnar absorptive epithelial
Nutrigenomics
Nutrigenomics refers to the study of the effects of how diet (food and food
constituents) may alter an individual’s gene expression and encompasses
nutritional factors that protect the genome from damage.8 Interactions
between the diet and the genome can effect health and disease via many
interconnected pathways including RNA expression (transcriptome),
epigenetics modification (epigenome), intermediary metabolites (metabo-
lome), lipids (lipidome), proteins (proteome), and resident microbiological
communities in the gastrointestinal tract (microbiome).1 Nutrigenomics
uses functional omics technology (high pass-through technology) to probe
a biological system following a nutritional stimulus, which permits a better
changes that may alter gene expression but do not involve changes in the
primary DNA sequence. These include 3 distinct but closely interacting
mechanisms—DNA methylation, histone modifications, and noncoding
microRNAs (miRNAs) (Fig 1.2).10,11
Epigenetic mechanisms have been implicated in early nutritional pro-
gramming in utero or by early life environmental stimuli that cause adapta-
tions, such as a “thrifty phenotype” as a response to nutritional deprivation.
These adaptations may persist into childhood and adult years even though
Fig 1.2.
Epigenetic mechanisms: 3 major mechanisms for epigenetic alterations
in gene expression have been described. Reproduced with permission
from Zaid SK, Young DW, Montecino MA, et al. Mitotic bookmarking
of genes: a novel dimension to epigenetic control. Nature Rev Genet.
2010;11(8):583-589.11
DNA methylation
Methylated
promoter
Histone modifications
Inhibiting Activating
post-translational post-translational
modifications modifications
Nucleosome
Repressed Expressed
gene gene
Histone tail
Xa Xa Xa Xi
Both copies active Only one active
(Embryo) (Adult)
they are no longer needed (eg, when there is an abundance of food). The
persistence of this adaptation is thought to contribute to the development
of the metabolic syndrome in some adults. Similarly, changes in the nutri-
tional status of pregnant women in The Gambia in dry versus wet seasons
have been associated not only with changes in circulating maternal methyl
donor metabolites but also effect changes in DNA methylation patterns in
the genome of the exposed offspring.12
There is growing evidence that numerous dietary factors, including
micronutrients and nonnutrient dietary components, can modify epigene-
tic markers. As noted previously, in cases in which the altered dietary supply
of methyl donors effects DNA methylation, there are plausible explana-
tions for the observed epigenetic changes; however, to a large extent, the
mechanisms responsible for diet-epigenome-health relationships remain
to be discovered. Because there are approximately 1 million sites within the
human genome for DNA methylation to occur,13 specific epigenetic bio-
markers that cause disease versus those that are a consequence of disease
are hard to identify, even with high-passthrough technology.10
Nutrimetabolomics
Metabolomics offers great potential to understand how different dietary
nutrients affect metabolic pathways. Importantly, metabolomics can be
used to identify patterns of metabolic profiles among individuals that
reflect differences in dietary intake or identify individual metabolic activi-
ties that explain variation in dietary responses. Some have speculated the
metabolomics can be used to identify biomarkers of dietary intake that
overcome some of the shortcomings of dietary assessment tools, such as
dietary recalls or intake surveys.14 Characterizing the metabolome relies on
nuclear magnetic resonance (NMR) and mass spectrometry, coupled with
other separation techniques. Both lipids and proteins contribute signifi-
cantly to the metabolome.
Lipidomics uses mass spectrometry-based profiling to characterize
comprehensive lipid profiles. It is known that there is a strong relationship
between dietary fat intake, circulating lipids, and cardiometabolic outcomes
and the host’s genetically determined metabolism. Proteomics, character-
izing the post-translational modification of proteins with dietary exposure,
is very complex. Applications of proteomic technologies, including mass
spectroscopy with liquid chromatography, are necessary to understand
the relationships between dietary and genetic factors affecting health and
disease.1
Microbiomics
It is not possible to consider nutrigenetics and nutrigenomics without a
consideration of the microbiome. As a contributor to systems biology (see
below), the trillions of microorganisms that inhabit the gastrointestinal
tract represent a reservoir of genetic material that is significantly greater
than that of the human genome, with great interindividual variability. As
many as 9.9 million genes have been identified from a database of micro-
biota.15 Changes in the microbiome are greatly affected by diet, which
appears to be a major short- and long-term regulator of structure and
function of the gut. Thus, it is not surprising that the microbial population
in each person is unique, although significant similarities can be found
among individuals living in the same environment or with similar dietary
and behavioral characteristics. Its functional capacity is relatively consis-
tent in healthy people with pathways involved in metabolism, fermenta-
tion, methanogenesis, oxidative phosphorylation, and lipopolysaccharide
biosynthesis.15
Microbiomics and omics technology allow for study of the complex inter-
actions between the human genome, the genome of the gut bacteria, and
functional consequences such as the response of the gut immune system
(the inflammasome2). The gut microbiome performs many metabolic
activities not encoded by the human genome, including producing energy
from “nondigestible” carbohydrates, producing a number of water-soluble
B vitamins, modulating the immune system, influencing lipid metabolism
(small-chain fatty acids) including adipogenesis, and affecting the coagula-
tion system via the synthesis of vitamin K2 (menaquinones). The study of
interaction of the diet and the microbiota is an intense area of investigation,
and the effect of the microbiome on nutritional health will, without a doubt,
prove to be of great importance.16
References
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and gene-environment interactions: new directions in cardiovascular disease
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2. Kanneganti T-D. The inflammasome: firing up innate immunity. Immunol Rev.
2015;265(1):1–5
3. van der Greef J, Hankemeier T, McBurney RN. Metabolomics-based systems
biology and personalized medicine: moving towards n = 1 clinical trials?
Pharmacogenomics. 2006;7(7):1087–1094
4. Simopoulos AP. Nutrigenetics/nutrigenomics. Ann Rev Public Health. 2010;31
(1):53–68
5. Lucock MD. Synergy of genes and nutrients: the case of homocysteine. Curr Opin
Clin Nutr Metab Care. 2006;9(6):748–756
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15. Lynch SV, Pedersen O. The human intestinal microbiome in health and disease.
N Engl J Med. 2016;375(24):2369–2379
16. O’Connor EM. The role of gut microbiota in nutritional status. Curr Opin Clin
Nutr Metab Care. 2013;16(5):509–516
17. Panagiotou G, Nielsen J. Nutritional Systems biology: definitions and
approaches. Ann Rev Nutr. 2009;29(1):329–339
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