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2
Accomplishments in the
Nutrition and Food Sciences
Throughout history, people have observed connections between food
and health. In 400 B.C., Hippocrates wrote of the relationship between
diet and health. One hundred years later, beriberi was described in Chi-
nese texts, as were other nutrient-deficiency diseases in early writings.
Hippocrates and GaTen often used the word diet, but the term nutrition
did not come into popular use until the latter half of the nineteenth
century. The concept of nutrition that human beings require a steady
intake of specific components of food in defined amounts is thus clearly
a modern one. Foocl science and technology are concerned with the ve-
hicle food in which essential and desirable food components are deliv-
ered to the body in adequate amounts and in safe, acceptable forms.
The earliest efforts in nutrition science are often attributed to Antoine
Lavoisier. This French chemist demonstrated in 1789 that oxygen breathed
in from the air is used by the body to produce carbon dioxide and water in
what we know today as the central metabolic process in which food is
"burned" to provide the energy needecl for all bodily functions. Lavoisier
showed that the amount of oxygen used was related to the amount of food
consumed and the amount of physical activity. Later, other scientists ob-
served that citrus fruits prevented scurvy, iodine prevented goiter, and
unmilled rice prevented beriberi. Canning was invented and added to the
processor's means of preserving foocl, along with the traditional fermenta-
tion, drying, and salting. Louis Pasteur developed the process of pasteur-
ization, which saved countless lives and provided milk in a safe and palat
27
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as
OPPORTUNITIES IN THE NUTRITION AND FOOD SCIENCES
able form. It was only early in this century, however, that scientists de-
fined human nutritional requirements, identifying the amino acids, vita-
mins, fatty acids, and minerals in foods essential to health. Diseases such
as scurvy, beriberi, rickets, and pellagra were found to be caused by vita
r. .
mln c ~etlclencles.
After World War II, people in the United States were generally eating
better, thanks to improved transportation systems (which made a wider
variety of foods available), home refrigeration, frozen foods, and nutrient-
fortified foods such as bread and milk. The war stimulated improvements
in dehydration, heat processing, and other technologies to minimize spoil-
age of food while maintaining quality and taste. Nutrient-deficiency dis-
eases became much less prevalent in the United States and other industri-
ali%ed countries.
For several decades, nutrition scientists have been examining the re-
lationships of modern dietary patterns to deadly chronic diseases such as
heart and blood vessel diseases, cancer, and diabetes. Responding to the
dietary guidelines developed by the nutrition community, food scientists
have developed a wide range of technologies to lower the fat, salt, and
sugar in food. In addition, they have developed and implemented a variety
of quality control procedures to make processed foods generally safe and
of high quality.
As the nutrition and food sciences have evolved and expanded in this
century, they have assumed a growing role in public policy. By 1979, the
federal government was involved in more than 350 programs to ensure an
adequate and safe food supply for consumers. These programs covered
areas such as support to farmers, food safety and regulation, food fortifi-
cation, food assistance, nutrition services and training, monitoring of food
intake and nutritional status, food and nutrition research, and food and
nutrition education.
In the past several decades, the federal government has become the
largest funder of research in the nutrition and food sciences, now contrib-
uting more than $400 million dollars annually. Much of that research is
conducted in academic laboratories at colleges and universities. The land-
grant colleges and universities (with their focus on agriculture, rural com-
munities, and the needs of consumers) have been largely responsible for
the growth of the nutrition and food sciences in the United States. Much
of the research in these disciplines has been conducted in departments of
animal science, food science, and nutrition in schools of agriculture and
home economics. Increasingly, research on diet's role in chronic disease is
conducted by scientists in medical schools and schools of public health.
Fundamental nutrition research is now conducted as well in more general
university and professional school departments. Today, government at all
levels, the private sector (particularly the food industry), biomedical re
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ACCOMPLISHMENTS IN THE NUTRITION AND FOOD SCIENCES
29
searchers, health-care practitioners, foundations, and others are working
individually and together to support research in the nutrition and food
sciences, to bring the fruits of that research to the public, and to use it to
develop programs and policies that will improve the health of the public.
As we rapidly approach a new century, new challenges in the nutrition
and food sciences are emerging. Research opportunities that await us in-
clude defining and determining "optimal" nutrition (ensuring maximal health
and resistance to disease throughout the lifespan), determining the role of
nutrition in the expression of our genetic material, learning the role of
important substances in food (such as fiber and carotenoids) that are not
traditional essential nutrients, and developing more effective strategies
for promoting healthful dietary change. To meet these new challenges,
the science of human nutrition is becoming more interdisciplinary, draw-
ing on food science, biochemistry, molecular biology, genetics, physiology,
toxicology, epidemiology, and the social and behavioral sciences (such as
sociology, psychology, anthropology, and political science) to understand
the role of human nutrition in health and disease.
EXAMPLES OF ACCOMPLISHMENTS AND CHALLENGES
In the remainder of this chapter, we present examples of how re-
search in the nutrition and food sciences has led to discoveries and appli-
cations that have substantially improved the health and well-being of people
throughout the world. Chapters 3 through 6 describe future research on
·. - 1 1 11
1 ~
portun~es anct cnai~enges that stem from these accomplishments.
There are many examples that might be chosen to illustrate the ac-
complishments of the nutrition and food sciences. The following eight are
representative examples and are organized around three topics: the inter-
actions of genes with nutrients, improving the food supply, and nutrient
delivery and nutritional assessment. Further research in each of these
areas is likely to result in improved health, greater resistance to disease,
and better treatments for disease.
- 1
Gene-Nutrient Interactions
Iron
Iron, a constituent of hemoglobin in red blood cells, is essential for
carrying oxygen from the lungs to all the body tissues. Several crucial
enzymes involved in general metabolism require iron as well. Iron defi-
ciency remains one of the most common nutritional deficiencies around
the world. Groups most subject to deficiency are pregnant women, in-
fants, children, and menstruating women. Iron deficiency impairs physical
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OPPORTUNITIES IN THE NUTRITION AND FOOD SCIENCES
NOBEL PRIZES FOR RESEARCH APPLICABLE TO THE
NUTRITION AND FOOD SCIENCES
The Nobel Prize, established by Alfred Nobel at the turn of the
century to honor "those who . . . shall have conferred the greatest
benefit on mankind," is perhaps the most prestigious award one can
receive for one's work in certain fields. We list here Nobel laureates in
physiology or medicine and in chemistry whose work falls within the
nutrition and food sciences.
Year Name
1902 Emil Herman Fischer (Germany)
1904 Ivan P. Pavlov (Russia)
1923 Si r Frederick G. Banting (Canada)
and John ].R. MacLeod (Canada)
1928 Adolf O.R. Windaus (Germany)
1929 Christiaan Eijkman (Netherlands)
and Sir Frederick G. Hopkins
(Britain)
1929 Sir Arthur Harden (Britain) and
H. von Euler-Chelpin (Sweden)
1934 George R. Minot, William P.
Murphy, and George H. Whipple
(U n ited States)
1937 Sir Walter Norman Haworth
(Britai n)
1937 Paul Karrer (Switzerland)
1937 Albert Szent-Gyorgy (Hungary)
1938 Richard Kuhn (Germany)
1943 Henrik Dam (Denmark) and
Edward A. Doisy (United States)
Accomplishment
Research on the synthesis of
sugars and purines
Work on the physiology of
. .
d ~gest~on
Discovered the hormone
. , .
Insulin
Research on sterols and their
connection to vitamins
Discovered the antineuritic
vitamin (thiamin) and several
growth-stimulating vitamins
Investigated the fermenta-
tion of sugars by yeast juice,
leading to later studies of the
basic metabolic processes of
life
Discoveries concerning liver
therapy against anemia (Years
later, it was shown that vita-
min B12, found in liver, could
prevent or treat pernicious
anemia.)
Research on carbohydrates
and vitamin C
Research on carotenoids and
vitamins A and B
Research on basic metabolic
processes, with an emphasis on
. . _
vitam ~ n _
Research on carotenoids and
. .
vltamlns
Discovery of vitamin K and
research on its chemical
natu re
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ACCOMPLISHMENTS IN THE NUTRITION AND FOOD SCIENCES
1945 Arttu ri Vi rtan en (Fi n Ian d)
1947 Carl F. Cori and Gerty T. Cori
(United States)
1953 Sir Hans Adolf Krebs (Britain)
and Fritz A. Lipmann
(United States)
1955 Vincent Du Vigneaud
(United States)
1957 Sir Alexander Robertus Todd
(Britain)
1964 Konrad Bloch (United States) and
Feodor Lynen (Germany)
1964 Dorothy Crowfoot Hodgkin
(Britain)
1965 Robert Bu rns Woodward
(United States)
1967 George Wald (United States)
1970 Luis F. Leloir (Argentina)
1982 Sune K. Bergstrom (Sweden),
Bengt 1. Samuelsson (Sweden),
and John R. Vane (Britain)
1985 Michael S. Brown and
loseph L. Goldstein
(United States)
Development of several inven-
tions in agriculture and nutri-
tional chemistry, especially a
method to preserve fodder
Research on glycogen and
. .
Its conversions by enzymes
Discovery of the citric acid
cycle in the metabolism of
carbohydrates
Studies on the biochemistry of
sulphur compounds and con-
tributions to knowledge about
the vitamin biotin
Research on nucleotides and
their coenzymes (Early in his
career, he synthesized thiamin
and worked on vitamins E and
B12.)
Research on the metabolism
of cholesterol and fatty acids
Determined the structure of
vitamin B12
Developed techniques for
synthesis of organic molecules
including cholesterol, chloro-
phyll, and vitamin B12
Research on vision and the iden-
tification of a vitamin A me-
tabolite as the critical mole-
cule of the visual pigment
rhodopsin
Discovered sugar nucleotides
and their role in the biosyn-
thesis of carbohydrates
Research on the biochem-
istry and physiology of pros-
taglandins
Research into the regulation
of cholesterol metabolism and
the development of cholesterol-
related diseases
31
a,
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OPPORTUNITIES IN THE NUTRITION AND FOOD SCIENCES
and work performance as well as immune function. Sustained deficiency
eventually leads to anemia.
Pregnant women me nf~rhnnc the most at rick nnn''l~ti~n in this Ron_
~ . ~ lo. . ~ ~ ~ .
try tor Iron aeticlency. Iron deficiency and anemia during pregnancy-
which are more common in African-American women and those of low
socioeconomic status, with multiple gestations, and with limited educa-
tion may be harmful to the fetus, but the data are not conclusive. Iron
deficiency is of special concern for infants and young children because it
may affect permanently their physical and mental development. Infants
with even mild iron deficiency anemia have impaired ability to attain skills
that involve mental and muscular activity, such as crawling, talking, ant!
solving cognitive problems. It is not clear whether these psychomotor
delays are ever completely reversed after the deficiency is corrected. In
children, iron deficiency can cause apathy, short attention span, irritabii-
ity, and reduced ability to learn. Iron deficiency also increases the risk of
lead toxicity, which can impair cognitive function permanently. Iron (lefi-
ciency is linked with increased concentrations of lead in the blood of
preschool children.
In contrast, dietary iron toxicity is rare in this country. Several hun-
dred children each year experience acute iron poisoning from iron supple-
ments, mistaking them for candy. People who carry a gene from both
parents (who are homozygous) for hemochromatosis may experience chronic
iron toxicity from consuming iron in food. lIemochromatosis is a heredi-
tary disorder of iron metabolism that results in the slow accumulation of
iron in the tissues. The primary defect appears to lie in the intestine.
Intestinal iron absorption is abnormally high, resulting in excess iron be-
ing absorbed from food and supplements. If not identified and treated,
hemochromatosis can lead to cirrhosis, cardiovascular disease, diabetes,
arthritis, impaired immune function, cellular damage (since excess iron is
an oxidant that attacks the fat molecules in cell membranes), and possibly
liver cancer. While these clinical features represent the end point of a
chronic condition of iron overload, children as young as two years of age
with this disease may have high concentrations of iron in their blood.
lIemochromatosis is believed to be the most common inherited metabolic
disorder, with 1 in every 400 to 500 individuals possibly having both genes
and being likely to develop the disease. The responsible gene has not
been identified. Nutrition scientists are eager to understand this abnor-
mality of iron absorption and to explore the molecular mechanisms of iron
absorption in normal individuals (see Chapter 31.
There is no definitive biochemical marker in the body to diagnose
hemochromatosis. The usual method of screening for this disorder in a
general population is to draw blood to identify individuals with markedly
elevated concentrations of ferritin (the form of iron stored in tissues) or
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ACCOMPLISHMENTS IN THE NUTRITION AND FOOD SCIENCES
33
elevated transferrin saturation (a test of the protein that carries iron in the
blood). Where possible, these individuals should have the presumptive
diagnosis confirmed with a follow-up liver biopsy. The treatment for this
disorder is to bleed patients periodically, which removes some red blood
cells and forces the body to use some of its stored iron as it replenishes its
supply of these cells.
Given the relatively high prevalence of hemochromatosis in the U.S.
population, it is clear that there are many more people who carry a
hemochromatosis gene from one of their two biological parents (that is,
who are heterozygous for this gene). These carriers a group that may
represent as many as 10 percent of people in the United States are at
increased risk of some of the diseases caused by hemochromatosis. lIow-
ever, blood tests to determine iron status are not sensitive enough to
distinguish between heterozygotes for hemochromatosis and normal indi-
viduals. Research is needed to develop noninvasive screening tools to identify
the large population of these heterozygotes. Research leading to the iden-
tification of the hemochromatosis gene and the metabolic products of its
expression could open new vistas both for identifying affected individuals
and for improving the treatment.
The prevalence of iron deficiency in the United States and the risks of
iron overload to a significant minority raise important public policy ques-
tions and pose significant challenges for intervention. The iron fortifica-
tion policies of this country have been very effective in combating iron
deficiency, but we must be vigilant to ensure that iron-fortified foods
reach those populations at high risk of deficiency without putting those
with hemochromatosis, or those prone to the disorder, at risk. An alterna-
tive approach involves identifying the 10 percent of the population that
may be at increased risk of iron overload and learning whether they need
to decrease their iron intake.
Energy Balance and the Risks of Diabetes and Obesity
Diabetes exists in various forms, but they all have in common abnor-
mal metabolism of carbohydrates, which leads to hyperglycemia (excess
sugar, or glucose, in the blood). Non-insulin-dependent diabetes mellitus
(NIDDM), the most common form of this clisease, occurs when the body
loses its ability to respond to insulin, the hormone produced by the pan-
creas to lower blood sugar concentrations. NIDDM is linked to obesity
for reasons that are unclear. Researchers assume that at least some obe
sity-associated diabetes results from the interaction of the genetic back-
grounds of populations and specific genetic traits in individuals, along
with a variety of lifestyle factors, including what and how much one eats.
These interactions are undoubtedly behind the high prevalence of obesity
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OPPORTUNITIES IN THE NUTRITION AND FOOD SCIENCES
and diabetes among certain populations, such as the Pima Indians in the
Southwest.
NIDDM has a strong genetic basis. Several gene mutations linked to
NIDDM have been identified recently, including 40 different mutations
of the insulin receptor on cells. (This receptor binds insulin, one of sev-
eral compounds the body uses to control blood glucose concentrations,
and thereby lets glucose into the cells.) Although obesity is also influ
ence(1 by genes, no specific human gene mutation has yet been identified.
To study the contribution of genetic background and lifestyle to obe-
sity, researchers have developed inbred strains of animals that are either
very susceptible or very resistant to this disorder. As a result, there is an
immense amount of information on the metabolic derangements and al-
tered patterns of behavior that accompany the various forms of genetic
obesity in animals. To date, however, we do not know the series of events
that leads from the presence of a known gene or a specific experimental
manipulation (e.g., feeding diets high in fat or sugar) to the development
of full-blown obesity.
Scientists are using cellular and molecular genetic techniques to iden-
tify and isolate genes that promote obesity in laboratory rodents. One
animal mode! shows sex-related differences in obesity-associated diabetes.
The model is relevant to humans because when men and women are
matched for bocly fatness, men are clearly at greater risk for diabetes.
Studies suggest that diabetes is linked to the distribution of body fat (where
in the body it tends to collect) as well as to how much there is.
The type of obesity associate(1 with diabetes and its complications is
called central, or android, obesity. In this type, the enlarged fat cells are
found primarily in the abdomen. Where in the abdomen the fat is found-
just under the skin (subcutaneous) or deeper (visceral) also affects the
risk of disease. The more benign form of obesity is known as gynoid
obesity, in which excess fat is deposited mainly in the hips and thighs.
Obese men tend toward android obesity; obese women are of both types.
flow the distribution of excess body fat influences metabolism and the
risks of disease is unclear, but stimuli (such as the concentrations of sex
hormones) have different effects on fat cells depending on where in the
bocly they are. Much more research is needed to define the link between
distribution of body fat, insulin resistance, the influence of sex hormones,
and the risk of diabetes and other chronic diseases.
As will be (1iscussed in Chapters 3 and 5, many opportunities exist to
study the underlying causes of these two disorders, particularly the mechanisms
through which genetic and dietary factors interact. Progress will be made
toward this goal through further research on inbred strains of animals and
by using transgenic animals (animals into which DNA from a different
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ACCOMPLISHMENTS IN THE NUTRITION AND FOOD SCIENCES
35
species of animal or plant has been inserted; see section on biotechnology
later in this chapter).
Folate and Neural Tube Defects
During this century, we have learned much about the biochemistry
and physiology of vitamins in relation to human nutritional requirements,
but we continue to learn more. For example, foods or vitamin supple-
ments containing the B vitamin folic acid, taken prior to and during the
first trimester of pregnancy, can prevent some neural tube defects (NTDs)-
birth defects in which the spinal column does not close during embryonic
development.
We hypothesize that NTDs result from interactions between the genes
of the developing embryo and its intrauterine environment. The genetic
component, which probably involves several genes, is complex and not
well understood. Epidemiological studies (in which population groups are
compared) and other evidence indicate a strong environmental compo-
nent as well. The nature of these environmental factors, especially the
supposed role of micronutrients (vitamins and minerals), is not well un-
derstood. Animal models support the hypothesis that vitamin deficiencies
contribute to some human NTDs.
Growing evidence from observational and intervention studies in hu-
mans suggests that supplements of folic acid t0.1 to 4.0 milligrams (mg)
per day] taken around the time of conception (one to three months before
conception and during the first six weeks of pregnancy) can reduce the
risk of NTDs. On the basis of these studies, the federal government has
recommencled that fertile women consume 0.4 mg of folic acid each day,
slightly more than twice their current recommended dietary allowance
(RDA). While it is not difficult to obtain this amount from food with a
well-selected diet, most women fail to do so.
More research is needed to determine the amount of folic acid that
prevents NTDs most effectively, to learn the molecular mechanisms by
which folic acid reduces the incidence of NTDs, and to determine the
risks to the population at large of significantly increasing folic acid intake.
It is known that folic acid converted to forms that participate in reactions
that lead to DNA synthesis. Therefore, it may prevent delays in DNA
synthesis, delays in fetal development through abnormal expression of
genes, and thus the failure of the neural tube to form completely.
Recommendations have been made to fortify foods with folic acid so
that all women capable of becoming pregnant can more easily consume
0.4 mg per day in their diets. However, this strategy presents some diffi-
cult public policy issues, because it would lead to most of the public
consuming significantly more folic acid than they do now, and this could
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OPPORTUNITIES IN THE NUTRITION AND FOOD SCIENCES
pose risks to some. For folate, as for most nutrients, we know little about
the Tong-term effects of ingesting considerably more than the RDA, par-
ticularly in forms that are very well absorbed by the body. We have no
information about how ingesting 1 or more mg of folic acid dafly over
months and years may affect inclivicluals with conditions that may predis-
pose them to unanticipated harmful effects. For example, approximately
one-quarter of the elclerly population may be at risk for vitamin B 2 clefi-
ciency because their ability to absorb BE from foods or supplements is
impaired. Since folio acid masks the characteristic anemia of vitamin Big,
deficiency, widespread fortification of foods with this nutrient could per-
mit vitamin BE deficiency to go undiagnosed.
We encourage reaclers interested in this topic to peruse Chapter 5,
which presents many opportunities for investigating the role of nutrition
and its relation to various pregnancy-relatec3 outcomes and conditions ant!
the Tong-term consequences of nutritional insults and inadequate nutri-
tion on early development. Chapter 6 provides a discussion of the re-
search opportunities in assessing growth, development, and nutritional
status, as well as understanding the motivations for and barriers to chang-
ing food habits.
Oxidative Damage to DNA, Proteins, anc] Fats
Research using methods that range from the test tube to an entire
population suggests that forms of oxygen procluced in our bodies in the
course of daily living can cause significant damage, affecting the aging
process and increasing our risks of a variety of chronic diseases. These
"active oxygen" species include singlet oxygen ant] oxygen raclicals con-
taining an unpaired electron, which makes them likely to interact with
important molecules in the body and produce undesirable by-products.
For example, oxidizecI genetic material (DNA) can initiate or promote the
development of cancers of the lung, colon, breast, and uterus ant! cause
chromosomal abnormalities. Oxidative damage to proteins is linked to the
formation of cataracts. Oxidized fatty acids and the products formed from
them are linked to damage to the arteries leading to the buildup of fatty
plaques. Oxi(lative damage caused by active oxygen species also may com-
promise the immune system.
Given the constant, inevitable production of active oxygen species, it
is no surprise that the body has evolved mechanisms to prevent their
damaging consequences, some of which are influenced by what we eat.
The enzymes superoxide dismutase (which contain essential trace miner-
als such as copper, manganese, and zinc) en cl glutathione peroxiclase (which
contains the essential trace mineral selenium) provide two such mecha-
nisms to inactivate these forms of oxygen. Many carotenoids (including
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ACCOMPLISHMENTS IN THE NUTRITION AND FOOD SCIENCES
37
those that are precursors of vitamin A) can quench singlet oxygen, and
vitamin E can prevent the propagation of oxygen radical-initiatecT reac-
tions. Vitamin C regenerates vitamin E that has become oxidized in the
course of fighting oxidation, thereby contributing to the efficacy of this
fat-soluble vitamin. Several studies of population groups link low intakes
and low blood concentrations of these antioxidant nutrients with several
diseases, including heart disease, several cancers, and cataracts of the eye.
Evidence of health benefits from supplements of these nutrients is sug-
gestive but not yet convincing.
Each of the diseases mentioned above has important genetic compo-
nents. The predisposition to coronary heart disease that occurs in middle
age can be explained in significant measure by genetic disorders that in-
volve the transport of cholesterol ant! other fats in the bloocT. However,
the known risk factors unclerlying heart disease (such as high bloocI cho-
lesterol, high blooci pressure, and cigarette smoking) fad! to account for
much of the individual susceptibility to this major cause of death in the
United States. Although there is considerable evidence that oxidation of
blood lipoproteins within the arterial wall, particularly the low-density
lipoproteins (LDLs) that carry most of the cholesterol in the blood, un-
derTies the early development of atherosclerotic plaques, the factors that
regulate formation of oxidized LDL are still largely unknown. That such
factors could be critical is supported by observations that the susceptibil-
ity of inclividuals with familial hypercholesterolemia, a common genetic
disease, to the development of coronary heart disease varies widely among
families and cannot be explained simply by the concentrations of LDL in
the blood. What may underlie these differing susceptibilities are impor-
tant interactions between nutrients and genes that are influenced by diet
or how the body metabolizes critical nutrients. Similarly, the genetic de-
terminants of metabolism and the way the hotly handles various nutrients
may underlie some of the genetic susceptibility to other chronic diseases
that can develop as a result of oxidative damage.
The fact that one's genetic endowment can influence the aging pro-
cess is suggested by observations in the fruit fly. Strains specially bred to
be long-lived tend to have a more active form of the enzyme superoxicle
dismutase. In one strain into which genetic material was inserted, leading
the flies to produce greater than normal amounts of this enzyme, the
average life span (though not the maximum life span) was increased.
These examples provide some indication of the types of research in
antioxidant biology that have considerable potential to improve human
health. For further details, see Chapter 3.
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OPPORTUNITIES IN THE NUTRITION AND FOOD SCIENCES
Improving the Food Supply
Sensory Biology and the Development of New Foods
The typical person in the United States derives more than one-third
of his or her daily calories from fat and one-fourth from sugars, both
natural and added. Fat and sugar together account for more than one-half
the total daily energy intake. Diets low in carbohydrate and fiber but rich
in simple sugars and fat are linked to a high prevalence of obesity and
increasect risk of chronic disease, including coronary heart disease, diabe-
tes, and some forms of cancers. Excessive fat intake has been called the
number-one problem in the U.S. diet, and current dietary guidelines rec-
ommend reducing fat consumption to 30 percent or less of total calorie
intake.
Reclucing fat consumption is no easy task. We generally like the taste
of high-fat foods and are reluctant to give them up. EIigh-fat diets are
flavorful, varied, and rich. Fats are largely responsible for the texture,
mouthfeel, and flavor of many foods anc] play an important role in deter-
mining the palatability of the cliet. Poor adherence to low-fat regimens is
a clocumented problem in the dietary management of people with high
cholesterol counts, while cravings for sweet, high-fat foods are a major
obstacle to weight reduction. Even highly motivated cardiac patients often
find it difficult to follow diets composed of grains, vegetables, fruit, and
low-fat dairy products.
One approach to implementing dietary guidelines is to apply existing
strategies and models of behavior change to the dietary behavior of com-
munities and populations. The National Cholesterol Education Program is
a classic example of this approach to lower total fat, saturated fat, and
cholesterol consumption in this country. Another approach to implement-
ing dietary guidelines is to after the available food supply, because dietary
compliance may increase if low-fat foods offer the same eating pleasure as
foods high in fat. Recent advances in food technology, particularly the
development of fat-replacement products, offer one way of reducing fat
consumption while satisfying natural sensory preferences for a varied, pal-
atable diet. Similarly, the use of intense sweeteners offers a way of reduc-
ing excess sugar consumption.
Sensory preferences for sweetness and fat are deeply ingrained and
appear to be universal. The pleasure response to sweetness is innate and
has been observed in human infants at birth. The pleasure response to
fats is most likely learned early on; sensory preferences for high-fat foods
have been observed in children, adolescents, and adults. The pleasure
response to palatable foods may involve central brain mechanisms. The
neurotransmitter serotonin and endogenous opioid peptides may mediate
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39
preferences for carbohydrates, sugar, and fat. Taste preference profiles
for sugar-fat mixtures also change with age and may be modified further
by repeated cycles of weight loss and gain.
At the same time, large-scale epidemiological and agricultural studies
suggest that the amount of fat in the typical diet is strongly influenced by
socioeconomic factors. Indeed, the amount of fat in the typical Western
diet may be influenced not so much by physiological variables as by the
amount of fat available in the food supply. Consequently, strategies for
reducing fat consumption must be planned carefully.
The food industry has made impressive progress in increasing the
range of palatable yet low-fat products available to consumers. One prom-
ising area is the production of leaner beef, leaner pork, and eggs with less
cholesterol. The food industry is using new technologies to develop new
generations of low-calorie or zero-calorie fat replacement products and
new versions of intense sweeteners.
Biotechnology
Since first domesticating plants and animals, people have exploited
the genetic diversity of living systems to improve the food supply. Over
the centuries, we have developed well-accepted techniques for selectively
breeding plants and animals for desirable characteristics. Producing fer-
mented foods such as cheese, bread, and wine in a wide variety of forms
depends on an ability to manipulate and alter microorganisms. Biotech-
nology provides a new set of tools for improving the variety, productivity,
and efficiency of food production and the nutritional quality of foods.
Genetic engineering provides a mechanism for producing specific genetic
improvements in plants, animals, and microorganisms in less time and
with greater precision, predictability, and control than possible with tradi-
tional methods of breeding and selection.
~. ~
, ~
Plants Genetic engineering can be used to improve dramatically the nu-
tritional quality of plants by making minor modifications in their genetic
makeup. For example, cereal grains, which are the main source of protein
for the vast majority of the world, are deficient in essential amino acids.
Improving their amino acid composition would make them a higher-qual-
ity, more complete source of protein. It is now possible to improve the
nutritional value of oilseeds, which supply almost half the fat in our diets.
Gene transfer technology has been used to alter composition and reduce
the degree of saturation of fatty acids
sunflower and safflower.
The many studies linking diet to cancer have led to research to iden-
tify the responsible components in food. Over 600 plant-derived chemi
in major oilseed crops such as
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OPPORTUNITIES IN THE NUTRITION AND FOOD SCIENCES
cats (phytochemicals) have cancer-preventing potential, including antioxi-
dants such as beta-carotene and vitamins C and E. In the future, genetic
engineering will make it possible to manipulate the amount of these chemicals
in food. In addition, plant tissue culture techniques may be used to pro-
duce phytochemicals that could be added to processed foods.
An emerging technology that promises to have a dramatic effect on
the genetic engineering of Plants involves inserting a single gene normaliv
v V ~ 1 0 ~ ~ ~
. . 1 . ~ _ ~
present in a plant in the opposite orientation. This antisense technology
has already been used to block the expression of single genes involved in
the ripening process in tomatoes (thereby reducing Tosses caused by pre-
mature spoilage) and in caffeine production in coffee beans. It coulc3 also
be used to block the production in food of antinutrients such as phytates
and oxalates, which bind to minerals and make them unavailable for ab-
sorption. By improving the taste, texture, and shelf life of fresh fruits and
vegetables, this technology should entice more consumers to eat more of
these nutritious foods.
Animals Genetic engineering will be increasingly important in animal
agriculture. The most obvious applications involve directly manipulating
an animaT's hotly composition, growth rate, and disease resistance. There
is also a growing interest in using transgenic animals (which have incorpo-
ratecl genetic material from an unrelated animal, plant, or microorganism)
to produce novel proteins in milk, blood, and urine that can be extracted
and purified.
Many complex biological processes affecting fertility, ratios of lean
meat to fat, growth rate, and milk yield are regulated by hormones. The
genes directing the production of many of these hormones have been
cloned, providing opportunities to manipulate the physiology of farm ani-
mals. For example, somatotropin (growth hormone) genes from several
animal species have been identified, characterized, and integrated into
the gene pool of related ancI unrelated animal species. Supplements of
bovine somatotropin (BST) improve the feed efficiency of cows and in-
crease their milk production without altering the milk's composition. Por-
cine somatotropin (PST) enables the pig to form muscle rather than fat,
dramatically reducing the fat content of pork.
Genetic changes that improve disease resistance and feed digestion
in foocl-producing animals will have an indirect but very positive effect on
the nutritional quality of their meat and milk. Several economically im-
portent diseases might be combated by transgenic strategies, thereby de-
creasing dependence on antibiotics and broad-spectrum chemical treat-
ments and reducing drug residues in the food supply. Genetic approaches
have been proposed to increase the digestive capacity of ruminant ani-
mals. One option is to add transgenic bacteria that produce digestive en
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ACCOMPLISHMENTS IN THE NUTRITION AND FOOD SCIENCES
41
zymes into the rumen of these animals. For example, enzymes called phytases
increase the availability of phosphorus, which is essential for forming bone,
in plant foods. Incorporating phytase-producing bacteria in the rumen of
cows, for example, would reduce both the amount of expensive phospho-
rus needed in their diet and the amount excreted in their feces. The latter
would reduce phosphorus contamination of grounc3water from farm wastes.
Food-processing biotechnology Bacteria, yeasts, and molds have been used
for centuries to produce fermented foods such as cheese, yogurt, sausage,
pickles, sauerkraut, wine, beer, soy sauce, and bread. Biotechnology can
be used to alter the metabolic processes of these microorganisms in ways
that will improve production efficiency and extend shelf life, improve
nutritional content, or ensure the safety of the product. Microorganisms
with a long history of safe use can be manipulated to produce food flavors
and flavor enhancers, sweeteners, thickeners, and nutritive additives such
as vitamins, amino acids, and fiber.
Biotechnology will enable us to develop systems that rapidly detect
pathogenic and spoilage organisms, microbial ant! fungal toxins, and chemical
and biological contaminants in foods. In addition, it wfl} provide innova-
tive ways of treating food-processing waste with microorganisms and en-
zymes to help prevent environmental contamination and convert some of
this waste to higher-value food and nonfooc3 products.
To make the most of biotechnology, we must learn much more about
metabolism in plants, animals, and microorganisms. Many opportunities
exist, for example, to study the biochemistry and genetics of carbohydrate,
protein, and fat metabolism. There is little doubt that this powerful tech-
nology wfll improve dramatically the nutritional quality of the food supply
in the coming years. (For further details, see Chapter 4.)
Preventing Chilclhoocl Morbidity and Mortality
Oral Rehydration Therapy
The development of oral rehydration therapy (ORT) represents a milestone
in the history of public health nutrition. Use of an oral solution containing
sugar and electrolytes to help replenish fluids lost during acute diarrhea
can be traced back thousands of years to traditional folk remedies and
non-western medical traditions. The scientific rationale for such a therapy
emerged with the recognition in the 1800s that the mortality associated
with cholera was due primarily to diarrhea and the resulting loss of body
fluids and electrolytes.
Basic research in the 1950s established the mechanisms by which
sodium and organic solutes are transported in intestinal cells. By the 1960s,
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OPPORTUNITIES IN THE NUTRITION AND FOOD SCIENCES
clinical studies of the effectiveness of ORT were being carried out in
several Asian countries. These were followed by studies that confirmed
the efficacy of oral rehydration and extended it as a therapy to patients
suffering from acute diarrhea of any origin.
Diarrhea is the most frequent cause of death of young children in the
world. To combat this scourge, the World Health Organization (WHO) in
1971 formulated a simple and standard oral rehydration solution; it began
worldwide distribution of packets of this solution and instructions to pre-
pare the solution at home. Efforts to promote ORT have targeted the
household, as ORT is a simple, inexpensive primary health care interven-
tion that can be used effectively by family members. The initial mass
health education programs to encourage widespread use of ORT had only
limited success. Public health workers have learned that they must recog-
nize and work within the health beliefs and childcare practices of various
cultures if they are to succeed in increasing the acceptance and use of
ORT.
Vitamin A
The first scientific paper describing the discovery of vitamin A ap-
peared in 1913. Investigators soon learned that rats made deficient in this
nutrient stopped growing, became more susceptible to infections, and
died. Those that managed to survive the longest ultimately developed
xerophthalmia, a term for eye problems caused by vitamin A deficiency.
Human xerophthaImia is very dramatic; the most severe manifestation is
keratomalacia, in which the cornea literally melts, often in just a few
hours, causing blindness. Children who develop keratomalacia die at a
high rate, because they are not only severely deficient in vitamin A, but
also badly malnourished in general, usually suffering from respiratory dis-
eases and diarrhea.
For many decades, scientists and health workers focused on the ocu-
lar changes resulting from vitamin A deficiency. As a result, they did not
recognize or become sufficiently alarmed by the other potential conse-
quences of this deficiency, particularly in impoverished developing na-
tions. This situation began to change in the early 1980s after investigators
followed a group of 4,000 pre-school-age children in Indonesia who ap-
peared well-nourished and healthy, but who had night blindness and other
mild manifestations of xerophthalmia. Over time, the children with mild
xerophthalmia died at a greater rate than children whose eyes were clini-
cally normal at the beginning of the study. This association had a strong
dose-response relationship; that is, the more vitamin A-deficient the child,
the more likely he or she was to die, suggesting that the observation went
beyond mere coincidence. However, it was always possible that other,
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~3
unrecognized factors associated with vitamin A deficiency accounted for
the increase in the death rate (mortality). The next logical step was to
conduct controlled clinical trials to eliminate potential confounding fac-
tors and to determine whether reversing vitamin A deficiency could re-
duce mortality.
By 1993, these clinical trials had been conducted in several countries
in Southeast Asia, Africa, and Central America. The overwhelming con-
clusion based on the combined results is that improving vitamin A status
can reduce mortality, mainly from diarrhea and respiratory diseases, in
childhood by 25 to nearly 40 percent. In fact, some studies suggested that
the reduction in mortality might be as high as 72 percent if every child
targeted for vitamin A treatment had actually received all the treatments.
These phenomena are one side of an emerging equation. The other
side concerns measles-related mortality. Measles in Africa is a devastating
disease; it has a high mortality and is the major cause of blindness among
African children. Studies of children hospitalized for severe measles in
Africa have shown that providing vitamin A can save lives and reduce the
severity of sickness brought on by the disease. WHO and the United
Nations International Children's Emergency Fund (UNICEF) recommend
that vitamin A be routinely used to treat children with measles in all
countries where vitamin A deficiency is known to be a problem or where
the fatality rate from measles exceeds 1 percent.
Initiatives must be developed to ensure that all children get enough
vitamin A to prevent even subclinical deficiencies (those that are not readily
apparent). Among the initiatives proposed or already adopted are encour-
aging breastfeeding, promoting cultivation of foods rich in beta-carotene
(which the body converts to vitamin A), changing dietary habits, fortifying
commonly used ingredients, and providing supplements of vitamin A to
children to build up their stores of this nutrient in the liver.
We have learned that vitamin A supports the growth and development
of body tissues soon after conception and on through life. This nutrient is
also required for the health and integrity of the skin and other organs,
such as the lung and intestine, that help prevent microorganisms from
entering the body. Growing evidence points to the importance of vitamin
A and its metabolites (compounds the vitamin is converted into) and to
precursors of vitamin A (carotenoids such as beta-carotene) in maintain-
ing health and reducing the risk of certain cancers and possibly heart
disease. Yet we have much to learn about optimal intakes of vitamin A and
the carotenoids as well as the mechanisms by which they promote growth
and health. Exciting advances in molecular and developmental biology
described in Chapter 3 have led to the discovery that a metabolite of
vitamin A, retinoic acid, directs the expression of a large number of genes.
Future research will undoubtedly help us to understand how vitamin A
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OPPORTUNITIES IN THE NUTRITION AND FOOD SCIENCES
acts in organs throughout the body to maintain their health, control infec-
tion, and protect against various chronic diseases.
New Concepts of Nutrient Requirements
Nutrient requirements are currently defined as the amounts of nutri-
ents needed to maintain normal body functions. The most widely used
methods to determine requirements have been nutritional balance, or depletion-
repletion, studies. In such studies, the requirement for a nutrient was
assumed to be met if intake equaled output (i.e., balance) or if body
functions dependent on that nutrient remained "normal." Recently, we
have learned that nutritional balance can be achieved without maintaining
normal or optimal function. This was evident, for example, in studies of
zinc nutrition in lactating Amazonian women. Although their usual intake
of zinc was only S.4 mg per day (about two-thirds of the amount recom-
mended), they achieved a positive zinc balance by absorbing a high pro-
portion of the intake. When these women were given zinc supplements,
their milk supplied adequate zinc and larger amounts of vitamin A, and
their nursing infants had less risk of developing diarrhea. Apparently, the
usual zinc "balance" of these women was not without cost to them and
their infants in terms of other biological functions. We therefore cannot
assume that all zinc functions are fully met just because balance is achieved.
During the past decade, we have made significant advances in using
heavy isotopes as tracers to study the metabolism of nutrients. Methods
have been developed to administer these isotopes to humans, as have
analytical methods for measuring them in biological samples. These tech-
niques have enabled us to measure body stores, turnover, kinetics (move-
ment), and recycling of nutrients in people with very different eating
habits and physiological states (e.g., adolescence and pregnancy). It is now
possible, with the help of computers and appropriate software, to use this
information to develop mathematical models that depict the movement of
nutrients through the digestive system, into the bloodstream, and to spe-
cific sites within tissues. These kinetic models have been built for several
nutrients, including zinc, selenium, copper, calcium, and vitamins A and D.
A kinetic model can be used, for example, to determine whether par-
ticular dietary patterns place individuals at risk of depleting their body
stores of zinc by reducing zinc absorption from the intestine or increasing
its excretion in urine and sweat. An adequate zinc intake might be defined
as the amount required to maintain zinc stores at some specified level at
an appropriate rate of absorption from the intestine. A diet poor in zinc
could then be defined as one that leads to a drop in body stores or that
maintains body stores by forcing the body to substantially increase zinc
absorption or markedly decrease excretion. Dietary zinc requirements could
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45
then be formulated for a variety of different types of diets consumed
around the world, such as cereal-based (moderate-zinc) diets, red-meat-
based (high-zinc) diets, or poultry-based (low-zinc) diets. In this way we
can begin to individualize dietary zinc requirements and recommend in-
takes for populations based on their usual dietary patterns.
As we begin to think about possible changes in dietary allowances, we
must revisit the criteria for establishing requirements for all nutrients in
healthy people in a manner similar to that described above for zinc. Also,
these same models and novel approaches can be used to study nutrient
requirements of people with various diseases. For example, the wasting
syndrome associated with acquired immunodeficiency syndrome (AIDS)
places those patients at particular nutritional risk. They could be studied
using isotopic tracers to determine how this clisease alters nutrient bal-
ance. However, apart from the relevance of such research to specific dis-
eases, learning how disease disrupts nutrient balance can provide new
insights into nutrient metabolism in health.
We have learned a great deal about our vulnerability to specific nutri-
ent deficiencies and the detection and consequences of these deficiencies
based on a quarter century of experience in delivering nutrients to indi-
viduals with various diseases who cannot eat normally. These patients
require nourishment delivered entirely through a vein (total parenteral
nutrition) or with synthetic formulas either by mouth or via a tube in the
stomach or intestine (enteral nutrition). Some receiving this specialized
form of nutrition support have developed nutrient deficiencies particu-
larly of trace minerals such as zinc, copper, selenium, molybdenum, and
chromium that are often clinically dramatic. The good news, however, is
that identifying these deficiencies has enabled investigators to determine
the essentiality and practical importance of these trace minerals in human
nutrition and to design more effective formulations. For example, studies
of patients fed entirely intravenously have provided the only evidence that
humans are vulnerable to a dietary deficiency of molybdenum and some
of the strongest evidence that chromium deficiency may impair our ability
to metabolize carbohydrates properly.
It is in providing specialized nutrition support that we have also de-
tected deficiencies of vitamins, minerals, essential fatty acids, and certain
amino acids. The amino acid glutamine is one such example. Glutamine is
not regarded to be a dietary essential because it can be synthesized in
adequate quantities by our muscles. It then enters the blood circulation
and is taken up, in part, by other tissues where it is needed, especially the
immune system, kidneys, and the cells lining the intestine. The intestine,
which uses glutamine as a source of energy, derives what it needs in part
from the diet, as this amino acid is present in protein-containing foods. A
patient fed entirely by vein will depend entirely on the supply from his or
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OPPORTUNITIES IN THE NUTRITION AND FOOD SCIENCES
her muscle, as the present generation of intravenous amino acid prepara-
tions does not contain glutamine. Patients receiving this form of nutri-
tional support who experience trauma or infection may not make enough
glutamine in their muscles to meet their needs.
Enteral and parenteral nutrition will become increasingly important
in the nutritional management of patients with a variety of disabling dis-
eases and medical problems. Continuing research in this area in both
animals and humans should yield further insights into the occurrence and
consequences of deficient and excessive intakes of various nutrients.
In the future, it may be possible to use functional tests of nutrient-
dependent functions to establish nutrient requirements, either alone or in
conjunction with other endpoints (such as body stores or turnover rates).
For example, since we need adequate zinc in our diets to detect and
discriminate various tastes, requirements for zinc might be defined as the
amount that maintains taste acuity and enables the body to store a specific
amount of the mineral. In addition, we may wish to broaden the criteria
for establishing dietary allowances to encompass the goal of maximizing
healthy lifespans through the prevention of chronic diseases and by slow-
ing the aging process. Earlier in this chapter, for example, we noted that
antioxidant nutrients such as vitamins C and E consumed in adequate
amounts from food or taken as supplements might help to protect against
heart disease, several cancers, and cataracts. Clinical trials are needed to
determine the levels of intake of nutrients and other biologically active
constituents in food (such as dietary fiber and carotenoids) that enhance
health and reduce the risk of disease. (For further details, see Chapter 6.)
CONCLUDING REMARKS
In the next four chapters, we describe in detail a variety of current
and future opportunities for exciting and challenging research to advance
the nutrition and food sciences and to meet critical human needs. Many
of these opportunities stem from the accomplishments described above.
Chapter 3 presents opportunities in the basic biological sciences appli-
cable to nutrition, followed by food science and technology in Chapter 4.
In Chapter 5, we present opportunities in clinical nutrition research, fol-
lowed by Chapter 6 on public health nutrition. Some opportunities in
these latter two areas are clearly dependent on technological advances,
but many also depend upon research in basic biology and food science.
Representative terms from entire chapter:
folic acid
