Pocket Atlas of Nutrition E-Book

Hans Konrad Biesalski

• Herausgeber: Thieme
• Kategorie: Fachliteratur
• Sprache: Englisch
• Veröffentlichungsjahr: 2005

Seitenzahl: 467

Beschreibung

<p><fontcolor="red"><strong><em>Concise, practical, and designed for quick reference.</em></strong></font></p><p>With obesity and diabetes assuming alarming epidemic proportions, diet and nutrition are in the spotlight more than ever before. It has never been more important for health care professionals to be well informed, not only about the latest developments, but also about the scientific facts. <em>The Pocket Atlas of Nutrition</em> is an accessible guide to all aspects of nutrition, from basic chemistry to the most recent dietary guidelines.</p><p>Includes:</p><ul><li>More than 150 easy-to-understand, full-color plates <li>A comprehensive list of nutrients, including for each its composition, effect, function, occurrence and daily requirements, as well as recommended intake <li>An extensive listing of all vitamins, minerals, trace elements as well as non-nutritive substances with their function and interaction <li>Accessible discussions of special diets as well as nutritional recommendations for various medical conditions and throughout the life course, e.g. for pregnant women or athletes <li>Up-to-date coverage of food-related diseases, including BSE, genetically modified foods, food quality, food allergies, and functional foods</li></ul><p>We are bombarded by new information and claims about nutrition every day. <em>The Pocket Atlas of Nutrition</em> -- concise, practical, and designed for quick reference -- is an ideal basic guide for professionals and interested lay readers alike.</p>

Leseprobe

Pocket Atlas of Nutrition

Hans Konrad Biesalski, M.D.

ProfessorInstitute of Biological Chemistry and Nutrition SciencesUniversity of HohenheimStuttgart, Germany

Peter Grimm, Ph.D.

Institute of Biological Chemistry and Nutrition SciencesUniversity of HohenheimStuttgart, Germany

With the cooperation of Susanne Nowitzki-Grimm, Ph.D.

Translated and adapted for the American market by Sigrid Junkermann, M.S., B.A., Adj. Asst. Prof. of Biology and Nutrition, F.I.T., SUNY

177 color plates

ThiemeStuttgart · New York

Library of Congress Cataloging-in-Publication Data

Biesalski, Hans Konrad[Taschenatlas der Ernährung. English]Pocket atlas of nutrition/Hans Konrad Biesalski, Peter Grimm;with the co-operation of Susanne Nowitzki-Grimm; translation and adaption to theAmerican market by Sigrid Junkermann. –Rev. translation of 3rd German ed.p.; cm.Includes bibliographical references andindex.ISBN 3-13-135481-X (alk. paper) –ISBN 1-58890-238-2 (alk. paper)1. Nutrition–Handbooks, manuals, etc.2. Nutrition–Atlases.[DNLM: 1. Nutrition–Handbooks.]I. Grimm, Peter, M.D. II. Title.QP141.B5413 2005613–dc222004028350

1st German edition 19992nd German edition 20021st French edition 2001

This book is an authorized and completely revised translation based on the 3rd German edition published and copyrighted 2004 by Georg Thieme Verlag, Stuttgart, Germany. Title of the German edition: Taschenatlas der Ernährung

Translator: Sigrid Junkermann, New York

The color plates have been prepared by: M. Waigand-Brauner, U. Biesalski, and K. Baum

© 2005 Georg Thieme Verlag,Rüdigerstrasse 14, 70469 Stuttgart,Germanyhttp://www.thieme.deThieme New York, 333 Seventh Avenue,New York, NY 10001 USAhttp://www.thieme.com

Cover design: Cyclus, StuttgartTypesetting by Satzpunkt Ewert, BayreuthPrinted in Germany by Appl, Wemding

ISBN 3-13-135481-X (GTV)

ISBN 1-58890-238-2 (TNY)                                                                                                          1 2 3 4 5

EISBN 9781604061062

Important note: Medicine is an ever-changing science undergoing continual development. Research and clinical experience are continually expanding our knowledge, in particular our knowledge of proper treatment and drug therapy. Insofar as this book mentions any dosage or application, readers may rest assured that the authors, editors, and publishers have made every effort to ensure that such references are in accordance with the state of knowledge at the time of production of the book.

Nevertheless, this does not involve, imply, or express any guarantee or responsibility on the part of the publishers in respect to any dosage instructions and forms of applications stated in the book. Every user is requested to examine carefully the manufacturers’ leaflets accompanying each drug and to check, if necessary in consultation with a physician or specialist, whether the dosage schedules mentioned therein or the contraindications stated by the manufacturers differ from the statements made in the present book. Such examination is particularly important with drugs that are either rarely used or have been newly released on the market. Every dosage schedule or every form of application used is entirely at the user’s own risk and responsibility. The authors and publishers request every user to report to the publishers any discrepancies or inaccuracies noticed. If errors in this work are found after publication, errata will be posted at www.thieme.com on the product description page.

Some of the product names, patents, and registered designs referred to in this book are in fact registered trademarks or proprietary names even though specific reference to this fact is not always made in the text. Therefore, the appearance of a name without designation as proprietary is not to be construed as a representation by the publisher that it is in the public domain.

This book, including all parts thereof, is legally protected by copyright. Any use, exploitation, or commercialization outside the narrow limits set by copyright legislation, without the publisher’s consent, is illegal and liable to prosecution. This applies in particular to photostat reproduction, copying, mimeographing, preparation of microfilms, and electronic data processing and storage.

Foreword

The important role of nutrition in promoting health and preventing disease is well established. Although scientific understanding of the roles of various nutrients in human health has progressed rapidly over the past century, nutritional deficiencies remain a threat to the lives and health of millions of people throughout the world, particularly children. At the other end of the nutritional spectrum, a global epidemic of obesity is also threatening the lives and health of millions. Despite appearances, overweight and obesity are often associated with poor nutrition. Although poor nutritional status has long been associated with increased risk of infectious disease, a large body of evidence now supports the association of poor nutrition with increased risk of noninfectious chronic diseases. Obesity is associated with an increased risk of several cancers, including colon cancer and postmenopausal breast cancer. It has been estimated that diet modification could potentially prevent as many as one third of cancers worldwide. Epidemiologists at Harvard have estimated that as much as 70% of stroke and colon cancer, 80% of coronary heart disease and 90% of type 2 diabetes could be prevented by a healthy diet, regular physical activity, and avoidance of smoking. After reviewing the large body of evidence linking diet and chronic disease risk, a number of expert panels have made surprisingly similar recommendations for a healthy diet:

• Achieve and maintain a healthy body weight

• Increase consumption of fruits, vegetables, legumes, and nuts

• Replace saturated and trans fats with unsaturated fats

• Replace refined grains with whole grains

• Limit sugar and salt intake

• Drink alcohol in moderation (if at all)

Although basic to health, the study of nutrition is complex and integrates knowledge from disciplines as varied as physiology, molecular biology, chemistry, psychology, sociology, economics and public policy. In this edition of the Pocket Atlas of Nutrition. Professors Biesalski and Grimm are providing health and nutrition professionals, students and motivated consumers with a useful nutrition resource that is broad in its scope yet concise in its delivery. The first section of the book provides the reader with an important foundation in nutrition science, including essential topics such as body composition, energy requirements, appetite regulation, and the physiology of nutrient digestion and absorption. Subsequent chapters on macronutrients (carbohydrates, proteins and fats) and micronutrients (vitamins and minerals) discuss relevant clinical issues, as well as current intake recommendations. A section on nutrition in specific life situations addresses important nutritional issues specific to the elderly, pregnant and lactating women, young children, and athletes, while a section on nutritional medicine provides additional information on the role of nutrition in chronic disease prevention and treatment. Throughout the book detailed figures clarify and expand on information discussed in the text.

Unlike some nutrition texts, the Pocket Atlas of Nutrition does not shy away from controversy. In addition to presenting the often-criticized U.S. Department of Agriculture Food Guide pyramid, the authors also discuss the merits of the Healthy-Eating Pyramid created by the Harvard School of Public Health and a pyramid based on the Mediterranean diet. Discussions of food quality, food additives and food safety that cover controversial topics from the genetic modification of foods to bovine spongiform encephalopathy (BSE) will be of interest to consumers and clinicians alike. Despite the fact that there is general agreement among scientists regarding the basic components of a healthy diet, the proportion of the population that actually follows these guidelines is relatively small. Although consumers are interested in the relationship between diet and health, many are confused about what they should eat and whether they should take supplements.

Contributing to this confusion are seemingly contradictory nutritional sound bites supplied by the news media and well-funded marketing campaigns from food, dietary supplement, and weight loss industries. Now, more than ever, there is a need for nutrition and health professionals who understand and communicate consistent and accurate information regarding healthy diets and lifestyles. The Pocket Atlas of Nutrition will be a useful study guide and an excellent reference for those who want to learn more about the science of nutrition.

Jane Higdon, Ph.D.

Linus Pauling Institute

Oregon State University

Corvallis, Oregon

Preface

After 30 years of advice to eat low fat, the United States, followed closely by many other, mostly but not exclusively, industrialized nations, is witnessing an unprecedented epidemic increase in obesity and diabetes, to name just two. The cost of these developments to the individual and to society is enormous, and the projected cost for the future staggering. It is evident that the increase in obesity and diabetes is strongly related to faulty nutrition. Proper nutrition is probably the most effective and cost-effective prevention for these and many other diseases, including most cancers.

It should be clear to anyone by now that proper nutrition involves much more than having three meals a day. The written media abound with nutritional advice and information. Many books promote often extremely controversial guidelines for weight loss and better health. Frequently, articles and books are based on unproven assumptions, anecdotal evidence, or single scientific studies that seem to point in one or the other direction. The reader who tries to make sense of it all tends to be utterly confused.

Yet, even though nutritional science is relatively young, it is a hard science and many aspects have been thoroughly researched. Our knowledge of other aspects, such as the functions and effects of many secondary phytochemicals, or the multiple interactions between many body chemicals during nutrition-related metabolism, is evolving continually. Nutritional science is an interdisciplinary endeavor based on chemistry, biology, physiology, and anatomy, which are often hard to understand and even harder to present in a condensed, easy to assimilate fashion.

So where can the interested layperson turn for information? Where do professionals dealing with nutritional questions, physicians, nurses, pharmacists, teachers, etc.—who often have little or no nutritional training—turn for easily accessible, reliable, up-to-date, and comprehensive information? Where can dietitians and nutritionists quickly look up scientifically sound and up-to-date information about a particular nutritional topic?

This is where the Pocket Atlas of Nutrition comes in. It provides well-presented basic knowledge and presents the state of the art of nutritional science today. Of course, it cannot provide the in-depth approach of textbooks of nutrition, nutritional medicine, and related fields. We are hoping, though, that the compact presentation of knowledge typical of Thieme’s Pocket Atlas series will provide the reader with quick insights and a relatively easy to obtain overview. If the book raises in the reader a skeptical attitude toward quickly drawn conclusions, that was our intent.

Recent advances in molecular biology have allowed nutritional science to advance rapidly, and the information resulting from this research is increasingly complex. Yet, even most recent research findings have been included in these chapters, sometimes still marked as open questions.

Nutritional science remains a work in progress. In tune with the latest concerns about public health, this edition includes several new chapters on preventive nutrition and more emphasis has been placed on nutritional medicine.

Hans Konrad Biesalski

Peter Grimm

Sigrid Junkermann (Translator)

As the translator and as a teacher of biology and nutrition, I found it an exciting endeavor to render this German book in English and adapt it to the American market. It made me research a number of topics, compare European with American conditions, deepen aspects of my knowledge, confirm and revise others, and overall gain a deeper insight into the state of the art and the present direction of nutritional science. I also wish to express my gratitude to Angelika Findgott of Thieme International for having found me and given me the opportunity to do this work, for being a great editor, collegial, wonderful, and fun to work with.

Sigrid Junkermann

The authors are glad to have secured the collaboration of Ms. Sigrid Junkermann for this English edition. She has not only produced an accurate translation of fine literary quality but has also, through her familiarity with American conditions and guidelines and her tireless commitment and dedication to the quality of the book, succeeded in adapting this edition optimally to the standard practice and terminology of English-speaking health care professionals.

We are grateful to the readers for suggestions and criticism, as well as for comments relating to the content.

H.K.B., P.G.

Contents

Introduction

Introduction

Preventive Nutrition: A Science in Flux

Preventive Nutrition: The Mediterranean Diet

The RDA and DRI

Assessing Current Status

Body Composition

Variable: Body Composition

Water in Body and Foods

Anthropometrics

Experimental Methods

Nutrient Compartmentalization: Cellular Distribution

Nutrient Compartmentalization: Distribution to the Organs–Homeostasis

Energy Metabolism

The Biochemistry of Energy Transfer

How Food Energy is Used

Individual Energy Requirements

Energy Requirements

Tissue-Specific Energy Metabolism

Control of Energy Metabolism

Food Intake

Regulation of Food Intake: Hunger and Satiety

Leptin

Stomach Function

Nutrient Uptake

Anatomy and Histology

Cellular Mechanisms

The Colon: Active and Passive Functions

Enterohepatic Circulation

Regulation of Digestion

Principles of Digestion

The Nutrients

Carbohydrates

Structure and Properties

Digestion and Absorption

Metabolism: Distribution and Regulation

Metabolism: Glucose Storage

Glucose Homeostasis: Insulin and Glucagon

Metabolic Homeostasis: Blood Glucose Aspects

Glucose Tolerance

Fructose and Galactose

Sugar Alcohols: Metabolism

Sugar Alcohols: Occurrence

Glycoproteins

Fiber: Structure

Fiber: Effects

Occurrence and Requirements

Lipids

Classification

Fatty Acids

Lipid Digestion

Absorption

Transport

LDL-Receptor-Mediated Metabolism

HDL Metabolism

Postprandial Lipid Distribution

Lipoprotein Lipase

Fatty Acids: Metabolism

Cholesterol: Biosynthesis

Cholesterol: Homeostasis

Regulatory Functions: Membrane Structure

Regulatory Functions: Eicosanoids

Regulatory Functions: Influence of Nutrition

Occurrence and Requirements

Proteins

Proteins as a Source of Nitrogen

Classification: From Chain to 3-D Structure

Essential Building Blocks: The Amino Acids

Digestion and Absorption

Metabolism

Amino Acid Homeostasis

Regulatory Functions: Endothelial Functions

The Blood-Brain Barrier

Protein Quality

Occurrence and Requirements

Fat-Soluble Vitamins

Vitamin A: Chemistry

Vitamin A: Uptake and Metabolism

Vitamin A: Functions

Vitamin A: Regulation of Gene Expression

Vitamin A: Occurrence and Requirements

β-carotenes: Chemistry and Metabolism

β-carotenes: Functions, Occurrence, and Requirements

Vitamin D: Chemistry and Metabolism

Vitamin D: Functions

Vitamin D: Occurrence and Requirements

Vitamin E: Chemistry and Metabolism

Vitamin E: Functions, Occurrence, and Requirements

Vitamin K: Chemistry, Metabolism, and Functions

Vitamin K: Occurrence and Requirements

Water-Soluble Vitamins

Ascorbic Acid: Chemistry, Metabolism, and Functions

Ascorbic Acid: Occurrence and Requirements

Thiamin: Chemistry, Metabolism, and Functions

Thiamin: Occurrence and Requirements

Riboflavin: Chemistry, Metabolism, and Functions

Riboflavin: Occurrence and Requirements

Niacin: Chemistry, Metabolism, and Functions

Niacin: Occurrence of Requirements

Pantothenic Acid: Chemistry, Metabolism, and Functions

Pantothenic Acid: Occurrence and Requirements

Biotin: Chemistry, Metabolism, and Functions

Biotin: Occurrence and Requirements

Pyridoxine: Chemistry, Metabolism, and Functions

Pyridoxine: Occurrence and Requirements

Cobalamin: Chemistry, Metabolism, and Functions

Cobalamin: Occurrence and Requirements

Folic Acid: Chemistry, Metabolism, and Function

Folic Acid: Occurrence and Requirements

Vitamin interactions

B Vitamin Interactions

Free Radicals: Formation and Effects

Free Radicals: Endogenous Systems

Free Radicals: Exogenous Systems

Vitamin-Like Substances: Choline and Inositol

Vitamin-Like Substances: Nonvitamins

Minerals and Trace Elements

Calcium: Metabolism and Functions

Calcium Homeostasis

Calcium: Occurrence and Requirements

Phosphorus

Magnesium

Sulfur

Sodium Chloride

Potassium

Iron: Metabolism

Iron: Functions

Iron: Occurrence and Requirements

Iodine: Metabolism

Iodine: Function and Deficiency

Iodine: Occurrence and Requirements

Fluorine

Selenium: Metabolism and Functions

Selenium: Occurrence and Requirements

Zinc: Metabolism and Functions

Zinc: Occurrence and Requirements

Copper: Metabolism and Functions I

Copper: Functions II, Occurrence, and Requirements

Manganese

Molybdenum

Chromium

Vanadium

Tin and Nickel

Cobalt, Boron, and Lithium

Silicon, Arsenic, and Lead

Other Nutrients, Additives, and Contaminants

Secondary Phytochemicals: An Overview

Secondary Phytochemicals: Effects and Activity

Nonnutritive Nutrients

Alcohol: Metabolism

Alcohol and Health

Alcohol and Nutrition

Herbs and Spices

Additives: An Overview

Sweeteners

Contaminants I: Nitrate/Nitrite

Contaminants II: Residues and Pollutants

Pre- and Probiotics

Functional Foods and Nutraceuticals

Food Quality

Quality Defined

New Methods for Quality Optimization I: Preservation

New Methods for Quality Optimization II: Genetic Modification

Nutrient Content, Processing, and Storage

Hygiene

Applied and Medical Nutrition

Nutritional Guidelines

Nutrition for Healthy People I

Nutrition for Healthy People II

Vegetarianism

Separation Nutrition

Outsider Diets

Nutrition in Specific Life Stages

Pregnancy

Lactation

From Neonate to Adolescent

Seniors

Athletes

Ergogenic Aids

Selected Issues in Food Safety

Drugs and Diet I

Drugs and Diet II

Prion Diseases

Prion Diseases in the U.S.

Creutzfeldt-Jakob Disease (CJD and vCJD)

Medical Nutrition

Eating Disorders

Underweight

Obesity

Diabetes Mellitus: Pathogenesis

Pathologies Associated with Diabetes Mellitus

Molecular Mechanisms

Pathologies of Fat Metabolism: Hyperlipoproteinemia

Therapy

Metabolic Syndrome: Insulin Resistance Syndrome

Osteoporosis

Age-Related Macular Degeneration (AMD)

Cancer

Chronic Inflammatory Bowel Disease (CIBD)

Appendix

Table of Measures

General References

Selected Websites

Figure Sources

Index

Abbreviations

11-β-OHSD

11-β-hydroxysteroid dehydrogenase

5HT

5-hydroxytryptamine

5-methyl-THF or H3C-PteGLU

5-methyl-tetrahydrofolic acid

AA

Amino acids

AAS

Amino acid score

ACAT

Acyl-CoA cholesterol acyl-transferase

Acetyl-CoA

Acetyl coenzyme A

ADH

Antidiuretic hormone

ADH

Alcohol dehydrogenase

ADI

Acceptable Daily Intake

ADP

Adenosine diphosphate

AGE

Advanced glycylation end products

AHEI

Harvard School of Public Health Alternative Healthy Eating Index

AI

Adequate Intake

ALDH

Aldehyde dehydrogenase

AMD

Age-related macular degeneration

AMDR

Acceptable Macronutrient Distribution Range

AMP

Adenosine monophosphate

AMR

Advanced meat recovery

AN

Anorexia nervosa

ANF

Atrial natriuretic factor

APHIS

Animal and Plant Health Inspection Service

ARAT

Acyl-CoA-retinol acyl-transferase

AREDS

Age-related eye disease study

Arg

Arginine

As

Arsenic

As2O3

Arsenic trioxide

Asp

Aspartic acid

ATP

Adenosine triphosphate

AUC

Area under the curve

B

Boron

BCCA

Branched chain amino acids

BIA

Bioelectrical impedance

BMI

Body mass index

BMR

Basal metabolic rate

BN

Bulimia nervosa

BRFSS

Behavioral Risk Factor Surveillance System (CDC)

BSE

Bovine spongiform encephalopathy

BV

Biological value

Ca

Calcium

CaBP

Calcium-binding protein

CAD

Coronary artery disease

CCK

Cholecystokinin

CCO

Cytochrome C oxidase

CDC

Centers for Disease Control

CE

Cholesterol esters

CETP

Cholesterol ester transfer protein

CH3-Pte

Methyl tetrahydrofolic acid

CIBD

Chronic inflammatory bowel disease

CJD

Creutzfeldt-Jakob disease

CLA

Conjugated linoleic acid

CM

Chylomicrons

Co

Cobalt

CoA

Coenzyme A

Cp

Ceruloplasmin

Cr

Chromium

CRALBP

Cellular retinalbinding protein

CRBP

Cellular retinolbinding protein

CRF

Corticotropin releasing factor

CRIP

Cysteine-rich intestinal protein

Cu

Copper

CuSOD

CuZn-Superoxide dismutase

CVD

Cardiovascular disease

CWD

Chronic wasting disease

Cys

Cysteine

DBP

Vitamin D-binding protein

DFE

Dietary folate equivalents

DLW

Doubly labeled water technique

DM

Diabetes mellitus

DRI

Dietary Reference Intakes

DT

Delirium tremens

EAR

Estimated Average Requirement

ECW

Extracellular water

EDRF

Endothelium-derived relaxing factor

EER

Estimated energy requirement

ER

Endoplasmic reticulum

F

Fluorine

F−

Fluoride

FA

Fatty acids

FABP

Fatty acid binding protein

FAD

Flavin adenine dinucleotide

FAE

Fetal alcohol effects

FAS

Fetal alcohol syndrome

FC

Free cholesterol

FDC

Follicular dendritic cell

FD&C

Federal Food, Drug, and Cosmetic (Act)

Fe

Iron

FEMA

Federal Emergency Management Agency

FFA

Free fatty acids

FMN

Flavin mononucleotide

G6P

Glucose-6-phosphate

GAG

Glycosaminoglycan

Gal

Galactose

GI

Glycemic index

GL

Glycemic load

GLC

Glucose

GlcNAc

N-acetyl-glucosamine

Gln

Glutamine

GLP-1

Glucagon-like peptide 1

GLU

Glutamate

GLU

Glucoronic acid

Gly

Glycine

GM

Genetic modification

GMP

Good manufacturing practices

GR

Glutathione reductase

GRAS

Generally Recognized As Safe

GSH-Px

Glutathione peroxidase

GST

Glutathione-S-transferase

GTF

Glucose tolerance factor

H2S

Hydrogen sulfide

H3BO3

Boric acid

H3C-Pte-GLU

Methyl-tetrahydrofolate

H4-Pte-GLU

Tetrahydrofolic acid

Hb

Hemoglobin

HCA

Hydroxy citrate

HDL

High-density lipoproteins

HEI

USDA Healthy Eating Index

HFCS

High fructose corn syrup

His

Histidine

HMB

Hydroxymethyl butyrate

HMG

Hydroxymethylglutaryl

HUS

Hemolytic uremic syndrome

I

Iodine

I−

Iodide

ICW

Intracellular water

IDDM

Insulin-dependent diabetes mellitus

IDL

Intermediate-density lipoproteins

IF

Intrinsic factor

IgG

Immunoglobulin G

IM

Intramuscular

IP

Inositol phosphate

IPP

Isopentenyl diphosphate

IRS

Insulin receptor substrate

IU

International units

IUPAC

International chemical nomenclature

K

Potassium

kcal

Kilocalories

LCAT

Lecithin cholesterol acyl-transferase

LDL

Low-density lipoproteins

Li

Lithium

LNAA

Long-chain neutral amino acids

LPL

Lipoprotein lipase

Lys

Lysine

MAO

Monoamine oxidases

MCL

Maximum contaminant level

MCT

Medium-chain triglycerides

MEOS

Microsomal ethanol oxidation system

Met

Methionine

MGP

Matrix Gla-proteins

MJ

Mega joule

Mn

Manganese

MnSOD

Manganese-SOD

Mo

Molybdenum

Molybdate

MSG

Monosodium glutamate

NA

Nicotinic acid

NAD+

Nicotinamide adenine dinucleotide

NADP

Nicotinamide adenine dinucleotide phosphate

NADPH

Dihydro-nicotinamide adenine dinucleotide phosphate

NE

Nicotinamide

Neo-DHC

Neohesperidine DHC

N-HDL

Nascent high-density lipoproteins

Ni

Nickel

NIDDM

Non-insulin dependent diabetes mellitus

NMN

Nicotinic acid mononucleotide

NO

Nitrogen monoxide

Nitrate

NO-R

S-Nitrosocysteine

NOS

NO synthase

NPU

Net protein utilization

NPY

Neuropeptide Y

nvCJD

new variant Creutzfeldt-Jakob disease

OP

Organophosphate

P

Phosphate

PAF

Platelet activation factor

PAH

Phenylalanine hydroxylase

PAI

Plasminogen activator inhibitor

PAL

Physical activity level

Pb

Lead

PDCAAS

Protein digestibility-corrected amino acid scores

PEM

Protein energy malnutrition

PER

Protein efficiency ratio

PG

Polygalacturonase

Phe

Phenylalanine

PI

Phosphatidyl inositol

PKC

Protein kinase C

PKU

Phenylketonuria

PL

Phospholipids

PL

Pyridoxal

PM

Pyridoxamine

PMN

Polymorphonuclear leukocytes

PP

Pellagra preventive

PPS

Pentose phosphate shunt

Prot-SH

Sulfur-containing proteins

PRPP

Phospho ribosyl-1-diphosphate

PRPP

5-Phosphoribosyl-1-diphosphate

Pte

Pteridine

PTP

Phospholipid transfer protein

PUFA

Polyunsaturated fatty acids

R

Retinol

RA

Retinoic acid

RAR

Retinoic acid receptors

rBGH

Recombinant human growth hormone

RBP

Retinol-binding protein

RDA

Recommended Dietary Allowances (U.S.)

RDA

Recommended Daily Amounts (UK)

RDI

Reference Daily Intake (U.S.)

RDI

Recommended Daily Intakes (Australia)

RE

Retinol Equivalents

RE

Esterified Retinol

RE

Retinyl ester

REM

Remnants

RFBPs

Riboflavin-binding proteins

RfD

Reference dose

RME

Receptor-mediated endocytosis

RNI

Reference Nutrient Intake (UK)

ROS

Reactive oxygen species

RPE

Retinal pigment epithelium

R-PteGLUn

Non-methylated pteroyl polyglutamate

SAD

Seasonal affective disorder

SD

Standard deviations

Se

Selenium

Selenite

Selenate

Ser

Serine

Si

Silicon

Sia

Sialic acid

SiO2

Silicon oxide

Silicate

Sn

Tin

SO2

Sulfur dioxide

Sulfite

Sulfate

SOD

Superoxide dismutase

SR material

Specified risk material

SRM

Specified risk material

TBG

Thyroxine-binding globulin

TDP

Thiamin diphosphate

TEF

Thermic effect of food

TfR

Transferrin receptors

TG

Triglycerides

TG

Triacyl glycerole

THFA

Tetrahydrofolate

Thr

Threonine

TSE

Transmissible spongiform encephalopathy

TTP

Thiamin triphosphate

TTR

Transthyretin

UCP1

Uncoupling protein 1

UDP-

Uridine phosphate

UL

Tolerable Upper Intake Level

USP

United States Pharmacopeia

UWL

Unstirred water layer

V

Vanadium

vCJD

Variant Creutzfeldt-Jakob disease

VLDL

Very low density lipoproteins

VO2+

Vanadyl

Vanadate

X5P

Xylulose-5-phosphate

XO

Xanthine oxidase

YOPI

Young, old, pregnant, and immunocompromised

Zn

Zinc

αTE

α-Tocopherol equivalents

Introduction

Introduction

Introduction

Human foods are made up of essentially six basic component types (five groups of nutrients and water), each of which has different functions in the body (A). Carbohydrates and lipids represent our main energy sources. Proteins, vitamins, minerals, and trace elements are essential for growth and development of tissues. Water, proteins, and vitamins are needed for metabolism as well as for its regulatory functions. While energy nutrients (carbohydrates, lipids, proteins) are partially interchangeable in terms of their use, vitamins, minerals, and trace elements always play very specific roles. Consequently, a lack of any of these components results in nutrient-specific—albeit not always symptomatic—deficiencies. The commonality of all nutrient deficiencies is that they interfere primarily with growth. Consequently, growth rates can be used to demonstrate the value of balanced nutrition. Here is an example: in 1880, only 5% of male college students were over 1.80 m (6 ft) tall, by 1955 that percentage had reached 30%. Improved availability of nutrients since the beginning of the twentieth century has greatly increased life expectancy. Even though theoretical “availability” is more than sufficient in industrialized countries today, major improvements may still be possible through adjustments of nutrient ratios. According to present knowledge, a nutrition that prevents disease can be described in the following simplified manner: lipids <35% (i.e., less than 35% of total calories consumed), and predominantly from plant sources; proteins ~15%, also predominantly from plant sources; and carbohydrates >55%, with a high fiber content. This means a reduction in foods from animal sources and consumption of a varied array of plant foods with a high proportion of fruits and vegetables, all minimally processed.

Such general recommendations are not sufficient, though, since there is great diversity among people (B). Nutrition professionals (nutritional scientists, home economists, dietitians, physicians, etc.) need detailed information about individual nutrients to do justice to all the complexity. For this reason, many countries have developed recommendations intended to represent basic guidelines for desirable nutrient intakes. In the U.S., these recommendations are issued by the Food and Nutrition Board under the National Research Council. The most recent ones, the Dietary Reference Intakes (DRI), were established in conjunction with the Canadian Health authorities.

As nutritional science evolves, these recommendations are revised periodically, and new findings challenge old ideas all the time. On the other hand, external factors are changing as well. Over the past decades, many occupations have progressively evolved towards lower levels of physical activity, and, in many cases, increasing income levels. These factors have a major impact on food choices and nutrient requirements.

Preventive Nutrition: A Science in Flux

Controversy is an integral part of nutritional science. Like many other aspects, preventive nutrition is a controversial issue. During the past decades, reducing fat intake while increasing carbohydrate intake was recommended across the world. These recommendations were based on the observation that, in the Western industrial nations, high fat intakes seemed to correlate with a high incidence of coronary artery disease. Even though many details about the effects of various fatty acids had been known since the sixties, the message was simplified to state “Fats are bad.” It was assumed that a general reduction in fat intake would automatically lead to a reduced load of saturated fatty acids. Thus, low-fat diets became a standard. The food industry gladly picked up on this message, especially in the U.S. where low-fat products have a high market-share. Admonitions that called this fat-free strategy arbitrary were published repeatedly, but remained largely unheard.

As early as three decades ago, some scientists proposed that a high carbohydrate intake—or rather the intake of high-glycemic index foods (see p. 68)—might lie at the root of many degenerative diseases. As early as 1972, the American physician Dr. R.C. Atkins proposed a nutritional revolution by recommending consumption of more fats and fewer carbohydrates. The recent publication of a new food pyramid by Harvard scientists (A) gives new support to his thesis.

While whole grain products should be part of every meal, all foods with a high glycemic index, like white bread, baked potatoes, polished rice, pasta, and sweets have been banned into the pyramid’s upper levels. Their approach differentiates between refined and whole, simple and complex carbohydrates, taking into account their glycemic index and glycemic load. Additionally, strict distinctions are drawn between various types of fatty acids: vegetable oils are placed at the base, milk products, butter, and red meat moved up. Micronutrient intakes appear to be suboptimal regardless of such “healthy” nutrition; hence, multivitamin and mineral supplements are recommended.

Government authorities have not yet subscribed to these opinions (B). Their recommendations still consider a high overall fat intake to be the main problem, while carbohydrate foods represent the basis of the pyramid. No distinction is made between foods with high and low glycemic loads. It remains to be seen whether the official recommendations on preventive nutrition will change based on these recent developments.

To emphasize preventive and therapeutic aspects of nutrition, they are highlighted with orange bars next to the text. The orange bars mark those passages that pertain to prevention or therapy, and clinical or nutritional medicine.

Preventive Nutrition: The Mediterranean Diet

Nutrition in accordance with the official guidelines could be considered as preventive, in spite of recent discussions about antioxidant vitamins, for instance. Nutrient data derived from scientific research provide an important foundation for institutional nutrition plans (e.g., hospitals, nursing homes); however, they are too abstract for the general consumer, who needs easy-to-apply nutritional recommendations. Translated into practical recommendations and compared to present intakes, a preventive nutrition should increase the consumption of whole grains, fruits, and vegetables, enhance the use of plant over animal fats, and reduce the intake of fried and refined foods, especially simple sugars.

The popularity of outsider diets teaches that recommendations are more successful and attractive if combined with a “lifestyle” image, as may be provided, for instance, by the “Mediterranean Diet” (A).

Mediterranean food consumption patterns with their high proportion of various vegetables, grains, plant oils (olive oil, in particular), fish, small amounts of animal fats and meat, largely coincide with present-day ideas about a preventive diet. As early as in the 1950s, the “Seven Countries Study” found that, compared to Northern Europe and the U.S., Mediterranean countries had very low levels of heart disease.

Persons whose data were collected in the 1950s and 1960s are still followed within the framework of this study. They show that in the Mediterranean, too, the amounts of saturated fatty acids consumed increase with increasing wealth, lessening the preventive properties of the diet. In principle, the traditional Mediterranean is largely transferable to Western industrialized nations, since a great variety of foods is available. The high level intake of monounsaturated (olive oil) and n-3-fatty acids (fish) can be achieved in part by consuming rapeseed (canola) oil, which contains both components.

The National “5 A Day for Better Health” program is the National Cancer Institute’s attempt to convince people to adopt a healthier nutrition. It propagates the simple principle of eating fruit or vegetables five times a day. Since these are recommended to be eaten “in addition,” restrictions—which people tend to dislike or reject—are not necessary. Also, the principle is easy to remember; and since fruit and vegetables are rich in water, the resulting satiety automatically leads to lower intakes of other foods. Alternatively (max. twice/day), fruit or vegetables juices may be taken instead. Whether the “5 A Day” campaign will achieve the desired reduction in nutrition-related diseases remains to be seen within the coming years and decades.

The RDA and DRI

Early recommendations for nutrient intakes date back to the mid-1800s when, in the Lancashire district in England, nutrient intake recommendations were established because of a famine. The purpose, however, was solely to ensure adequate minimal nutrient intakes for the population and the army. In 1941, the U.S. National Research Council first issued recommendations which had the goal of achieving “perfect health” in the population. These Recommended Dietary Allowances (RDA) were updated in five-year cycles.

In order to determine the RDA for a specific nutrient, its intake is determined in a representative sample population with no deficiency symptoms. The RDA are derived from the resulting Estimated Average Requirements (EAR). Where no or insufficient scientific data are available, an Adequate Intake (AI) is approximated. No RDA and consequently no Dietary Reference Intakes (DRI) are set for these nutrients.

The Energy RDA (for energy nutrients) are set at the mean intake of the reference groups. Actual energy requirements vary depending on activity levels. As opposed to many nonenergy nutrients, excessive caloric intake cannot be excreted and leads to weight gain. Since the DRI (2002), recommendations for energy nutrients are expressed as a range, the Acceptable Macronutrient Distribution Range (AMDR). The AMDR is the range of an energy-yielding macronutrient that is associated with reduced chronic disease while providing adequate levels of essential nutrients.

The Nutrient RDA (A) are set at two standard deviations (SD) above the EAR. The assumption is that this recommendation provides adequate intakes for 97.5% of the population, so that they develop normally and remain healthy. Since for the majority of people, an intake of 77% of the RDA is adequate, the RDA provide a safety margin. At levels below the RDA, metabolic integrity may be compromised. At levels above the RDA, the likelihood of a deficiency approaches zero.

For most nutrients, there is a large safety margin above the RDA (B). With the exception of selenium, adverse effects appear only at several times the RDA. These amounts are reflected in the Tolerable Upper Intake Levels (UL), above which toxicity becomes apparent. Toxicity symptoms may be mild or more severe (e. g., B6), depending on the nutrient. Even though excessive intake of some energy nutrients causes nutrient-specific degenerative symptoms, no UL were established for energy nutrients, since the relationship between intake and degree of disease is linear, and no threshold could be established.

The difficulty in establishing the RDA lies in the fact that they are by necessity based on estimates derived from representative samples of the population. The RDA represent adequate, but not necessarily optimal intakes. Increasingly, prevention of chronic disease rather than just deficiencies is taken into consideration when setting reference intakes. The representative samples do not necessarily account for individual needs based on age, nutritional status, genetic variability, drug use and abuse, etc. Therefore, the RDA are not a measure to determine where the nutrient supply becomes marginal for the individual.

There are presently a host of different nutritional recommendations issued by governmental and other agencies throughout the world (C).

Assessing Current Status

There are basically two types of nutritional assessments (A), each with a different method:

1. Assessment of nutritional status (effects of past nutritional intakes on the body) and

2. Dietary intake assessment (present nutritional intakes).

Nutritional status is often assessed through biochemical analysis. This works for specific nutrients for which there is a measurable indicator. Conclusions on the nutritional availability of iron, e. g., can be drawn from the amount of hemoglobin in the blood. Anthropometrics, i. e., body measurements (see p. 16), provide a more general measure. Besides height and body weight, determination of skin fold thickness has been gaining increasing importance. Anthropometric measurements represent cumulative results of many different factors and do not differentiate among the various nutrients. Clinical symptoms caused by nutritional deficiencies tend to become apparent very late. A long-term low iron supply, e. g., will eventually result in clinical symptoms like pallor and reduced performance levels—symptoms that could have been averted through early intervention.

Direct dietary intake assessment can be ongoing (prospective) or retrospective. With the weighing method, all foods consumed are actually weighed, whereas the protocol method uses amount estimates. The inventory method assesses the food consumption of an entire household by registering use of food items, as well as leftovers and waste. For example, a large amount of food is made available to a family and after a week the remainder subtracted from the initial amount. This method is not suitable for assessment of individual consumption since it does not permit any differentiation between individuals. The accounting method is used in some countries to assess household food consumption for statistical purposes. Selected households keep a record of all food items purchased.

Among the retrospective methods, the determination of food frequency is most simple to conduct. Subjects are asked how frequently they consume specific food groups. A diet history is more informative since additional factors like nutrition-related behaviors are also recorded. 24-hour recall presupposes good memory in the participants, as all food items consumed within 24 hours have to be recalled—including their amounts.

Food consumption can also be assessed indirectly through official agricultural statistics. This, however, does not permit differentiation among different segments of the population and does not account for waste.

The results of all methods presented naturally contain errors. In a study conducted with 140 participants (B), a 24-hour recall was compared with the “actual” observed food consumption. During the recall, all types of foods were regularly omitted or listed erroneously. Cooked vegetables were omitted in more than 50% of all cases, whereas sugar was listed erroneously in nearly 30% of all cases.

Body Composition

Variable: Body Composition

The human body is made up of several distinct components, which differ in their chemical and structural characteristics. The extracellular compartment consists of support structures like bone lamellae, tendons and ligaments, and the extracellular fluid systems, blood plasma, and lymph. The totality of cells can be viewed as distinct from fatty tissue, which serves either as energy reserve (fat deposits), or as structural support or building material, as in cheeks or in the soles of the feet. The latter will be broken down only in extreme cases of nutritional deficiency or during illnesses accompanied by consumption. The fat deposits, however, may be subject to rather extreme fluctuations.

The “elemental” composition of a 70 kg (154 lb) male shows that ~60% is water and 16% or more is fat. Besides carbon (C), hydrogen (H), and oxygen (O), the chemical elements nitrogen (N), calcium (Ca), and phosphorus (P) are the most abundant in terms of mass (A). Most other naturally occurring elements can also be found in the human body; however, their significance is often unknown. Chemical composition changes with age. These changes are most striking during the first year of life (B). While the water content drops rapidly, fat content, protein in muscle mass, and minerals, mostly in bone, increase.

More than half of the total body water is found inside the cells. The intracellular space is the site of cellular metabolism. As opposed to other fluid spaces, it is not homogeneous and its composition may differ greatly between different types of cells.

Water in Body and Foods

Homeostasis of the water balance (A) ensures stability of the water content. This stable balance is achieved through various hormonal feedback mechanisms in conjunction with osmoreceptors. The total average daily water intake results from a combination of drinking, intake of water contained in solid foods, and oxidation water. The latter is an end-product of the oxidative metabolism of energy nutrients. The oxidation of 1 g carbohydrate yields 0.6 ml of water; of 1 g protein, 0.42 ml; and of 1 g fat 1.07 ml. Based on a mixed nutrition, the average daily total amounts to 300 ml of oxidation water. According to the recently established Dietary Reference Intake (DRI), to be properly hydrated, women need to consume 2.7 l, men 3.7 l water/d. This applies to sedentary people in temperate climates. Higher temperatures or activity levels increase these requirements. No Tolerable Upper Intake Level (UL) has been established for water. In the average person, ~80% of water intake comes directly from fluids and ~20% from water contained in foods. Approximately 1.5 l is excreted through the urine. The kidneys can influence water balance by altering the rate of reabsorption. To ensure proper excretion of sodium, potassium, and urea, a minimum fluid excretion of 300–500 ml is needed. When no drinking water is available, the water loss through the kidneys can be minimized with appropriate nutrition. This means minimizing those foods that result in the formation of urinary excreted metabolites. For instance, lowering intake of protein and table salt results in a reduction of urea and sodium in the urine and, therefore, lowers the minimum urine volume required. In particular situations, e. g., for a prematurely born baby with kidney insufficiency, this mechanism becomes important. Water loss via skin and lungs amounts to 0.9 l/d. Increased respiratory frequency, as occurs in higher elevations, dry and warm surroundings, as well as during physical activity, can greatly increase these losses; 0.5 l/h may be lost via the skin alone in extreme situations. Concurrent loss of sodium takes place, decreasing, however, with regular training. If water loss exceeds 3 l/d, sodium loss needs to be replenished, as does water.

Human fluid requirement is, therefore, dependent on metabolic activity, as well as the environment (B). Small children have a significantly higher rate of energy metabolism compared to adults, causing a higher rate of respiration with greater water loss.

In the digestive tract, actual water intake is of lesser significance (C). Each day, ~8 l of fluids are released into the tract in the form of various secretions. Together with the fluids we drink, this amounts to over 10 l/d, all of which is reabsorbed except for 0.2 l. Diarrhea, vomiting, or increased secretions of saliva or bile acids can greatly increase water loss through feces.

The water content of foods (D) determines their energy content. In general, foods with lower water content have lower energy content. Many vegetables consist of >90% water, whereas isolated components like oil or sugar contain practically no water.

Anthropometrics

The Body Mass Index (BMI) provides a more accurate anthropometric measurement (A). It is calculated from body weight (kg) divided by the square of height (m2); hence the BMI unit is kg/m2. The desirable BMI is also age-dependent:

Age 19–24:

19–24

Age 25–34:

20–25

Age 35–44:

21–26

Age 45–54:

22–27

Age 55–64:

23–28

Above 64:

24–29

The BMI is the current standard for evaluating body weight since it correlates fairly well with total body fat and is rather independent of height. However, a man with a BMI of 27 kg/m2 may have a body fat content ranging from 10 to 31% of body weight. Not only fat, but muscle mass, extracellular water, and/or bone mass may contribute to high body weight. For instance, athletes frequently have a rather high BMI without large fat deposits. To address this inaccuracy, subcutaneous fat is measured. Theoretically, this could be done with an ultrasound device or through infrared spectroscopy. In everyday practice, however, measurement of skin fold thickness with precision calipers has proven valid. Among the four most commonly used skin folds, the fold above the triceps muscle is the most easily accessible and can be most reliably determined. Skin fold thickness measurement errors may result from nonhomogeneous fat distribution.

An additional measurement, waist-to-hip ratio (B), takes this into account. Waist circumference is measured while standing, between the lower edge of the lowest rib and the upper edge of the pelvis. The hip circumference is measured at the level of the greater trochanters. A ratio above 0.88 in women and above 1.0 in men indicates an android or abdominal fat distribution pattern, which is particularly closely associated with cardiovascular complications and other illnesses. If the ratio is low, the gynoid type prevails, with a lesser health risk. The waist-to-hip ratio is a particularly valuable tool for determining whether weight reduction is necessary in case of moderate overweight.

Experimental Methods

Bioelectrical impedance (BIA) is based on differences in conductivity between bodily tissues (A). Water-containing tissues have low impedance since they are highly conductive because of the presence of electrolytes. Fatty tissues have greater resistance, and cell membranes function as electrical condensers. Since electricity of different frequencies flows preferentially in different compartments, the measurement of impedance, combined with phase displacement, permits conclusions about the three compartments: fatty tissues, lean body mass, and water. BIA is considered to produce reliable and well-reproducible values for healthy people. The simplicity of the method’s use is advantageous: the four stick-on electrodes don’t bother the patient. However, changes in plasma electrolytes, use of diuretics, or dextrose infusions can greatly disturb the results.

Measurements of conductivity, like the BIA, are based on the different conductivities of different tissues. Since the person to be measured has to be placed inside a magnetic coil, the method is not practical as a routine.

Body composition can also be determined through various isotope dilution methods (B). These are used to determine just one compartment—total body water. The method is based on the assumption that fatty tissue is water-free and hence cannot take up any electrolytes. By additionally defining that lean body mass has a constant 73.2% degree of hydration, all three compartments can be determined through appropriate calculations. The most commonly used isotopes are deuterium oxide (2H2O), tritium-labeled water (3H2O), and the potassium isotopes 42K and 43K. The respective isotope is injected, losses are measured in urine, blood levels are measured after an equilibration phase, and the resulting dilution factor is used to determine total body water. Measurements of total body potassium using the 40K method differ somewhat. The isotope occurs naturally at a level of 0.0118% of body potassium and can be determined using a whole body counter. An assumption is made that potassium is found in lean body mass at a fixed concentration of 8 mmol/kg. Just as with the injected isotopes, this makes it possible to calculate all three compartments. Isotope measurements are also subject to errors. The assumptions mentioned do not apply to pathological conditions like sepsis, stress, malnutrition, or obesity.

Underwater weighing (C) is considered the standard for determining body fat. The subject has to be submerged under water. The displaced water in the vessel corresponds to the body volume. If the body weight is known, the density (D) (in g/cm3) can be calculated. Since body water has a constant density of 1.0 g/cm3, and the density of lean body mass and fat are also near constant, D can be used to estimate the respective proportions of the three compartments. Any change in density is interpreted primarily as a change in body fat content.

Nutrient Compartmentalization: Cellular Distribution

The distribution of carbohydrates, lipids, proteins, vitamins, and other elements and molecules in animal cells resembles that of human cells (A) while plant cells differ considerably (B).

In animal cells, carbohydrate reserves are stored as glycogen, and they can’t store much of it. Their role as an energy reserve is of lesser importance since energy stored as fat uses space much more efficiently. Plants, except in seeds, don’t have such problems of space and efficiency. They can, therefore, afford the uneconomic luxury of storing energy as large amounts of starch. Plant cell walls usually consist of polysaccharides, indigestible to humans, which are also called fiber or roughage.

Lipids are always found in fat droplets made of triglycerides or vitamin A esters. They are also found in all biological membranes, which consist mostly of phospho- and sphingolipids. Human and animal cell membranes also contain cholesterol. Plant cell membranes do not.

Proteins are found in all cells and throughout all compartments, as well as all extracellular fluids. This reflects their importance in the structure and function of all living things.

Most vitamins, minerals, and trace elements are associated with proteins and hence also found in all cell compartments. Plants contain intracellular organelles known as chloroplasts, not found in animal and human cells, which are the sites of photosynthesis. The structure of chlorophyll—the light absorbing molecule—resembles that of hemoglobin; however, whereas hemoglobin contains iron, chlorophyll has a magnesium ion in its center.

Even though nearly all nutrient types are present in all plant cells, their distribution varies greatly, depending on cell types. In a cereal grain, most vitamins and minerals (C) are found in the aleuron layer. This layer makes up just a few percent of the grain’s weight. The largest compartment of a grain, the endosperm, consists nearly exclusively of carbohydrate in the form of starch. The germ, on the other hand, is rich in vitamin B1, vitamin E, and lipids. Usually, the germ is removed during the milling process to increase the shelf life of flour since hydrolysis or oxidation of the lipids contained in it would affect taste over time.

The aleuron layer and the germ are theoretically the nutritionally most valuable components of a cereal grain. In reality, though, most people prefer the vitamin- and mineral-deficient white flour.

Animal cells have similarly diverse distribution patterns. Muscle cells contain a high percentage of protein, whereas liver cells are rich in vitamins A, D, B12, and folate. Fatty tissues consist mostly of lipids, with which vitamin E and carotenoids are associated.

Nutrient Compartmentalization: Distribution to the Organs—Homeostasis

Nutrient intake, loss, metabolism, and requirements are subject to considerable changes over time and between individuals. Even intake can never be constant. This is in spite of the fact that most foods are always available nowadays, due to extensive world trade. Other factors like age, gender, or a person’s state of health, lead to varying nutrient needs, different metabolization, and storage capacities.

The fact that none of the measurable parameters have a “normal” value is a result of the important impact of genetic variability: Instead, there is just a more or less narrow normal range. One of the causes is a certain variability of the amino acid sequence of proteins. For instance, there are several forms of hemoglobin, which differ in their oxygen-binding capacity. Under normal conditions this does not necessarily affect their physiological function. But in some cases (sickle-cell anemia, thalassemia) it does. A similar situation can be assumed to exist with regard to enzymes and transport proteins involved in nutrient metabolism. These variables, based on mostly intracellular conditions, need to be factored into the evaluation of individual nutrient requirements.

The amount of a particular nutrient in the blood plasma is usually not a good parameter for determining nutrient availability. Nevertheless, the body frequently uses plasma content of nutrients as internal reference value (A). Hormonal and nonhormonal mechanisms regulate uptake, excretion, and/or release from storage in such a way that the registered value in the plasma is equal to the internal reference value. The function of this homeostasis is to ensure adequate nutrient supply to those tissues that need them most urgently at a given time.

The example of vitamin A shows that these homeostatic mechanisms often preclude a simple assessment of nutrient availability from easily accessible compartments like blood (B). With a sufficient vitamin A supply, the vitamin A content of the liver—its main storage organ—is 300–1000 μg vitamin A/g. Serum content ranges between 50 and 90 μg/dl (with individual variations). Even if no more vitamin A is consumed, the blood level is maintained for 12–15 months during which the liver contents continue to decrease. A marginal deficiency in the serum is detectable only during the last stage, just before complete exhaustion of liver storage.

Additionally, the wide range of normal values makes it hard to interpret serum values. Consequently, a serum value within normal range is of no diagnostic value and cannot be used to infer the vitamin A status of the entire organism.

Energy Metabolism

The Biochemistry of Energy Transfer

The carbohydrates, fat, and proteins consumed are oxidized, and the energy that is released in the process is transferred to ATP (A).

The key substance for this energy transfer is acetyl-coenzyme A (acetyl-CoA). Carbohydrates are converted to pyruvate during glycolysis and then further to acetyl-CoA. The fatty acids resulting from hydrolysis of triglycerides are also broken down into this two-carbon key compound. Amino acids from proteins are either metabolized indirectly through a pyruvate stage or directly into acetyl-CoA. The resulting acetyl-CoA pool can either be used to build amino and fatty acids or enter the citrate cycle where it is oxidized for energy gain. During this process, carbon dioxide (CO2) forms when carbon atoms get oxidized; the coenzyme nicotinamide adenine dinucleotide (NAD+) is reduced to NADH and flavine adenine dinucleotide (FAD) is reduced to FADH2. These are subsequently reoxidized during oxidative phosphorylation, and the energy released in the process is stored as ATP energy. Organisms need a sophisticated respiratory apparatus for this purpose alone: oxygen has to be made available in order to oxidize NADH, and the CO2 resulting from oxidation of energy nutrients’ carbon atoms needs to be eliminated.

The energy metabolism’s major metabolic pathways share mutually interactive control mechanisms without which an efficient and self-regulated interplay of the energy pathways of carbohydrates, lipids, and proteins would be impossible. Energy use functions as an important control value, overall. Many enzymatic pathways of the energy metabolism are inhibited when a cell receives more energy than it needs. The second enzyme of the glycolytic pathway, phosphofructokinase-1, represents such an important regulatory enzyme for an early metabolic step. Its activity is inhibited by the energy-rich end product ATP, as well as by an intermediate, citrate.

A rapid energy transformation process is, therefore, necessitates the removal of the forming ATP through energy use, as well as sufficient supply of substrate and oxygen. Aerobic metabolism prevails when the two latter requirements are met. During physical activity it is unavoidable for the oxygen supply to be occasionally insufficient for the necessary energy transformation. This leads to incomplete performance of the last step, oxidative phosphorylation. Its substrate NADH builds up and in turn inhibits the citrate cycle upstream, leading in turn to a build-up of pyruvate, which inhibits glycolysis. Thus, the entire energy transformation is halted. The body has one alternative allowing it to extract a small amount of energy—even in this situation—converting pyruvate into lactate. While this is a deadend pathway, it removes pyruvate so that glycolysis can again produce at least a small amount of ATP. This anaerobic metabolism enables sudden, maximal muscle performance without any required preparatory steps.

How Food Energy Is Used

The adult body makes and uses ~85 kg (187 lb) of adenosine triphosphate (ATP) per day. The energy in ATP (A) is stored in the high-energy bonds between the phosphates; the terminal bond has the highest energy.

Hydrolysis of these bonds (B) yields ~8 kcal (33.47 kJ) per 1 mol of ATP under physiological conditions. Additional energy can be obtained by further breakdown of ADP (adenosine diphosphate) to AMP (adenosine monophosphate)—this reaction is of lesser significance, though. In a reversal of the above hydrolysis, the energy released during the metabolic breakdown of energy nutrients is used to synthesize ATP by attaching a phosphate group to ADP.

Even though in a healthy person about 95% of the energy nutrients consumed are absorbed, only part of that energy is converted into ATP energy (C).

Fifty percent of the metabolizable energy