Terms in this set (47)

Despite supplement advertisements that claim otherwise, the vitamins do not
provide the body with fuel for energy. It is true, though, that without B vitamins
the body would lack energy. The energy-yielding nutrients— carbohydrate, fat,
and protein—are used for fuel; the B vitamins help the body to use that fuel.
Several of the B vitamins—thiamin, riboflavin, niacin, pantothenic acid, and
biotin—form part of the coenzymes that assist enzymes in the release of energy
from carbohydrate, fat, and protein. Other B vitamins play other indispensable roles in metabolism. Vitamin B6 assists enzymes that metabolize amino acids.
Folate and vitamin B12 help cells to multiply. Among these cells are the red blood
cells and the cells lining the GI tract—cells that deliver energy to all the others.
The vitamin portion of a coenzyme allows a chemical reaction to occur; the
remaining portion of the coenzyme binds to the enzyme. Without its coenzyme,
an enzyme cannot function. Thus symptoms of B vitamin deficiencies directly reflect
the disturbances of metabolism caused by a lack of coenzymes. Figure 10-2
illustrates coenzyme action.
The following sections describe the roles of individual B vitamins and note
many coenzymes and metabolic pathways. Keep in mind that a later discussion
assembles these pieces of information into a whole picture. The following sections
also present the recommendations, deficiency and toxicity symptoms, and
food sources for each vitamin. For thiamin, riboflavin, niacin, vitamin B6, folate,
vitamin B12, and vitamin C, sufficient data were available to establish an RDA; for
biotin, pantothenic acid, and choline, an Adequate Intake (AI) was set; only niacin,
vitamin B6, folate, choline, and vitamin C have UL. These values appear in the
summary tables and figures that follow and on the pages of the inside front cover.
When a normal dose of a nutrient (levels commonly found in foods)
provides a normal blood concentration, the nutrient is having a physiological effect.
When a large dose (levels commonly available only from supplements) overwhelms
the body and raises blood concentrations to abnormally high levels, the nutrient
is acting like a drug and having a pharmacological effect. Naturally occurring niacin
from foods has a physiological effect that causes no harm. Large doses of nicotinic
acid from supplements or drugs, however, produce a variety of pharmacological effects,
most notably "niacin flush." Niacin flush occurs when nicotinic acid is taken in
doses only three to four times the RDA. It dilates the capillaries and causes a tingling
sensation that can be painful. The nicotinamide form does not produce this effect.
Large doses of nicotinic acid can effectively lower LDL cholesterol and triglycerides
and raise HDL cholesterol—all factors that help to protect against heart disease.4
As effective as niacin therapy is in improving blood lipids, however, it may not benefit
patients with heart disease whose blood lipids are already being controlled with
statin drugs.5 The use of niacin as a drug may benefit other patients, but its use
must be closely monitored. People with the following conditions may be particularly
susceptible to the toxic effects of niacin: liver disease, diabetes, peptic ulcers,
gout, irregular heartbeats, inflammatory bowel disease, migraine headaches, and
alcoholism. The nicotinamide form does not improve blood cholesterol levels.6
The brain and spinal cord develop from the neural
tube, and defects in its orderly formation during the early weeks of pregnancy
may result in various central nervous system disorders and death. Folate supplements taken 1 month before
concept ion and cont inued throughout
the first trimester of pregnancy can help
prevent neural tube defects. For this
reason, all women of childbearing age who
are capable of becoming pregnant should
consume 0.4 milligram (400 micrograms)
of folate daily—easily accomplished by
eating folate-rich foods, folate-for tif ied
foods, or a multivitamin supplement daily.
Because half of the pregnancies each year
are unplanned and because neural tube
defects occur early in development before
most women realize they are pregnant, the
Food and Drug Administration (FDA) has
mandated that grain products be fortified
to deliver folate to the US population.*
Labels on fortified products may claim that
" adequate intake of folate has been shown
to reduce the risk of neural tube defects."
Fortification has improved folate status in
women of childbearing age and lowered the
prevalence rate of neural tube defects, as Figure 10-11 (p. 318) shows.
Some research suggests that folate taken before and during pregnancy may
also prevent congenital birth defects, such as cleft lip and cleft palate, and neurodevelopmental
disorders, such as autism.12 Such findings strengthen recommendations
for women to pay attention to their folate needs.
Folate fortification raises safety concerns as well. Because high intakes of folate
can mask a vitamin B12 deficiency, folate consumption should not exceed
1 milligram daily without close medical supervision. The risks and benefits of
folate fortification continue to be a topic of current debate, especially given that
5 percent of the US population exceed the UL for folate.13
Folate deficiency impairs cell division and protein synthesis—
processes critical to growing tissues. In a folate deficiency, the replacement of red
blood cells and GI tract cells falters. Not surprisingly, then, two of the first symptoms
of a folate deficiency are anemia and GI tract deterioration.
The anemia of folate deficiency is known as macrocytic or megaloblastic
anemia and is characterized by large, immature red blood cells (see Fig ure 10-12).
Without folate, DNA damage destroys many of the red blood cells as they attempt
to divide and mature. The result is fewer, but larger, red blood cells that
cannot carry oxygen or travel through the capillaries as efficiently as normal red
blood cells. Since the implementation of folate fortification in the United States,
the prevalence of macrocytic anemia has decreased dramatically.19
Primary folate deficiencies may develop from inadequate intake and have
been reported in infants who were fed goat's milk, which is notoriously low in
folate. Secondary folate deficiencies may result from impaired absorption or an
unusual metabolic need for the vitamin. Metabolic needs increase in situations
where cell multiplication must speed up, such as pregnancies involving twins
and triplets; cancer; skin-destroying diseases such as chicken pox and measles;
and burns, blood loss, GI tract damage, and the like.
Of all the vitamins, folate appears to be most vulnerable to interactions
with drugs, which can also lead to a secondary deficiency. Some medications,
notably anticancer drugs, have a chemical st ructure similar to folate's
structure and can displace the vitamin from enzymes and interfere with
normal metabolism. Like all cells, cancer cells need the real vitamin to
mult iply—without it, they die. Unfor tunately, ant icancer drugs af fect
both cancerous cells and healthy cells, creating a folate deficiency for all
cells. Aspirin and antacids also interfere with the body's folate status: aspirin
inhibits the action of folate-requiring enzymes, and antacids limit the
absorption of folate. Healthy adults who use these drugs to relieve
an occasional headache or upset stomach need not be concerned, but
people who rely heavily on aspirin or antacids should be aware of the
nutrition consequences.
Vitamin B12 and folate are closely related: each depends on the
other for activation. Recall that vitamin B12 removes a methyl group to activate
the folate coenzyme. When folate gives up its methyl group, the vitamin B12
coenzyme becomes activated (review Figure 10-10 on p. 316).
The regeneration of the amino acid methionine and the synthesis of DNA and
RNA depend on both folate and vitamin B12.* In addition, without any help from
folate, vitamin B12 maintains the sheath that surrounds and protects nerve fibers and promotes their normal growth. Bone cell activity and metabolism also depend
on vitamin B12.
The digestion and absorption of vitamin B12 depends on several steps. In the
stomach, hydrochloric acid and the digestive enzyme pepsin release vitamin B12
from the proteins to which it is attached in foods. Then as vitamin B12 passes
from the stomach to the small intestine, it binds with a stomach secretion called
intrinsic factor. Bound together, intrinsic factor and vitamin B12 travel to the
end of the small intestine, where receptors recognize the complex. Importantly,
the receptors do not recognize vitamin B12 without intrinsic factor. The vitamin
is gradually absorbed into the bloodstream as the intrinsic factor is degraded.
Transport of vitamin B12 in the blood depends on specific binding proteins.
Like folate, vitamin B12 enters the enterohepatic circulation—continuously being
secreted into bile and delivered to the intestine, where it is reabsorbed. Because
most vitamin B12 is reabsorbed, healthy people rarely develop a deficiency
even when their intake is minimal.
The RDA for adults is only 2.4 micrograms of
vitamin B12 a day—just over two-millionths of a gram. The ink in the period at
the end of this sentence may weigh about that much. As tiny as this amount appears
to the human eye, it contains billions of molecules of vitamin B12, enough
to provide coenzymes for all the enzymes that need its help. Most vitamin B12 deficiencies reflect inadequate
absorption, not poor intake. Inadequate absorption typically occurs for
one of two reasons: a lack of hydrochloric acid or a lack of intrinsic factor. Without
hydrochloric acid, the vitamin is not released from the dietary proteins and
so is not available for binding with the intrinsic factor. Without the intrinsic factor,
the vitamin cannot be absorbed.
Vitamin B12 deficiency is common among the elderly. Many older adults
develop atrophic gastritis, a condition that damages the cells of the stomach.
Atrophic gastritis may also develop in response to iron deficiency or infection
with Helicobacter pylori, the bacterium implicated in ulcer formation. Without
healthy stomach cells, production of hydrochloric acid and intrinsic factor diminishes.
Even with an adequate intake from foods, vitamin B12 status suffers.
The vitamin B12 deficiency caused by atrophic gastritis and a lack of intrinsic factor
is known as pernicious anemia.
Some people inherit a defective gene for the intrinsic factor. In such cases, or
when the stomach has been injured and cannot produce enough of the intrinsic
factor, vitamin B12 must be given by injection to bypass the need for intestinal absorption.
Alternatively, the vitamin may be delivered by nasal spray; absorption
is rapid, high, and well tolerated.
Because vitamin B12 is found primarily in foods derived from animals, people
who follow a vegetarian diet may develop a vitamin B12 deficiency.21 It may take
several years for people who stop eating animal-derived foods to develop deficiency
symptoms because the body recycles much of its vitamin B12, reabsorbing it over
and over again. Even when the body fails to absorb vitamin B12, deficiency may
take up to 3 years to develop because the body conserves its supply. Neurological
degeneration, a sign of vitamin B12 deficiency, appears more rapidly in infants born
to mothers with unsupplemented vegan diets or untreated pernicious anemia.
Because vitamin B12 is required to convert folate to its active form, one of the most
obvious vitamin B12-deficiency symptoms is the anemia commonly seen in folate
deficiency. This anemia is characterized by large, immature red blood cells, which
indicate slow DNA synthesis and an inability to divide (see Figure 10-12, p. 319).
When folate is trapped in its inactive (methyl folate) form because of vitamin B12
deficiency or is unavailable because of folate deficiency itself, DNA synthesis slows.
First to be affected in a vitamin B12 or folate deficiency are the rapidly growing
blood cells. Either vitamin B12 or folate will clear up the anemia, but if folate is
given when vitamin B12 is needed, the result is disastrous: devastating neurological
symptoms. Remember that vitamin B12, but not folate, maintains the sheath that surrounds and protects nerve fibers and promotes their normal growth. Folate
"cures" the blood symptoms of a vitamin B12 deficiency, but cannot stop the nerve
symptoms from progressing. By doing so, folate "masks" a vitamin B12 deficiency.
Marginal vitamin B12 deficiency impairs cognition.22 Advanced neurological
symptoms include a creeping paralysis that begins at the extremities and works
inward and up the spine. Early detection and correction are necessary to prevent
permanent nerve damage and paralysis. With sufficient folate in the diet,
the neurological symptoms of vitamin B12 deficiency can develop without evidence
of anemia and the cognitive decline is especially rapid. Such interactions
between folate and vitamin B12 highlight some of the safety issues surrounding
the use of supplements and the fortification of foods. No adverse effects have
been reported for excess vitamin B12, and no UL has been set.
Vitamin C parts company with the B vitamins in its mode
of action. In some settings, vitamin C serves as a cofactor helping a specific enzyme
perform its job, but in others, it acts as an antioxidant participating in
more general ways.
As an Antioxidant Vitamin C loses electrons easily, a characteristic that allows it to
perform as an antioxidant. In the body, antioxidants defend against free radicals.
Free radicals are discussed fully in Highlight 11, but for now, a simple definition
will suffice. A free radical is a molecule with one or more unpaired electrons, which
makes it unstable and highly reactive. Antioxidants can neutralize free radicals by
donating an electron or two. In doing so, antioxidants protect other substances from
free radical damage. Figure 10-16 (p. 328) illustrates how vitamin C can give up electrons
and then accept them again to become reactivated. This recycling of vitamin C. is key to limiting losses and maintaining a reserve of antioxidants in the body.
Other key antioxidant nutrients include vitamin E, beta-carotene, and selenium.
Vitamin C is like a bodyguard for water-soluble substances; it stands ready to
sacrifice its own life to save theirs. In the cells and body fluids, vitamin C protects
tissues from the oxidative stress of free radicals and thus may play an important
role in preventing diseases.23 In the intestines, vitamin C enhances iron absorption
by protecting iron from oxidation. (Chapter 13 provides more details about
the relationship between vitamin C and iron.)
As a Cofactor in Collagen Formation Vitamin C helps to form the fibrous structural
protein of connective tissues known as collagen. Collagen serves as the matrix
on which bones and teeth are formed. When a person is wounded, collagen
glues the separated tissues together, forming scars. Cells are held together largely
by collagen; this is especially important in the walls of the blood vessels, which
must withstand the pressure of blood surging with each beat of the heart.
Chapter 6 describes how the body makes proteins by stringing together
chains of amino acids. During the synthesis of collagen, each time a proline or
lysine is added to the growing protein chain, an enzyme hydroxylates it (adds an
OH group), making the amino acid hydroxyproline or hydroxylysine, respectively.
These two special amino acids facilitate the binding together of collagen
fibers to make strong, ropelike structures. The conversion of proline to hydroxyproline
requires both vi tamin C and iron. Iron works as a cofactor in the reaction,
and vitamin C protects iron from oxidation, thereby allowing iron to perform its
duty. Without vitamin C and iron, the hydroxylation step does not occur.
As a Cofactor in Other Reactions Vitamin C also serves as a cofactor in the synthesis
of several other compounds. As in collagen formation, vitamin C helps in the
hydroxylation of carnitine, a compound that transports fatty acids, especially
long-chain fatty acids, across the inner membrane of mitochondria in cells. It
also participates in the conversions of the amino acids tryptophan and tyrosine
to the neurotransmitters serotonin and norepinephrine, respectively. Vitamin C
also assists in the making of hormones, including thyroxine, which regulates the
metabolic rate; when metabolism speeds up in times of extreme physical stress,
the body's use of vitamin C increases.
In Stress Among the stresses known to increase vitamin C needs are infections;
burns; extremely high or low temperatures; intakes of toxic heavy metals such
as lead, mercury, and cadmium; the chronic use of certain medications, including
aspirin, barbiturates, and oral contraceptives; and cigarette smoking. During
stress, the adrenal glands—which contain more vitamin C than any other organ
in the body—release vitamin C and hormones into the blood.* When immune system cells are called into action, they use a great deal of oxygen
and produce free radicals. In this case, free radicals are helpful. They act as
ammunition in an "oxidative burst" that demolishes the offending viruses and
bacteria and destroys the damaged cells. Vitamin C steps in as an antioxidant to
control this oxidative activity.
In the Prevention and Treatment of the Common Cold Vitamin C has been a popular
option for the prevention and treatment of the common cold for decades, but
research supporting such claims has been conflicting and controversial. Some
studies find no relationship between vitamin C and the occurrence of the common
cold, whereas others report modest benefits—fewer colds, fewer days, and
shorter duration of severe symptoms, especially for those exposed to physical
and environmental stresses. A review of the research on vitamin C in the treatment
and prevention of the common cold reveals a slight, but consistent reduction
in the duration of the common cold in favor of those taking a daily dose of
at least 200 milligrams of vitamin C. The question for consumers to consider is,
"Is this enough to warrant routine daily supplementation?"
Discoveries about how vitamin C works in the body provide possible links
between the vitamin and the common cold. Anyone who has ever had a cold knows
the discomfort of a runny or stuffed-up nose. Nasal congestion develops in response
to elevated blood histamine, and people commonly take antihistamines for relief.
Like an antihistamine, vitamin C comes to the rescue and deactivates histamine.
In Disease Prevention Whether vitamin C may help in preventing or treating cancer,
heart disease, cataract, and other diseases is still being studied, and findings
are presented in Highlight 11's discussion on antioxidants. Conducting research
in the United States can be difficult, however, because diets typically contribute
enough vitamin C to provide optimal health benefits.
For decades, vitamin C ranked at the top
of dietary supplement sales. How much vitamin C does a person need? As is true
of all the vitamins, recommendations are set generously above the minimum requirement
to prevent deficiency disease and well below the toxicity level (see
Figure 10-17).
The requirement—the amount needed to prevent the overt symptoms of
scurvy—is only 10 milligrams daily. Consuming 10 milligrams a day does not
saturate all the body tissues, however; higher intakes will increase the body's total
vitamin C. At about 100 milligrams per day, 95 percent of the population
reaches tissue saturation. (For perspective, 1 cup of orange juice provides more
than 100 milligrams of vitamin C.) Recommendations are slightly lower, based
on the amounts needed to provide antioxidant protection. At about 200 milligrams,
absorption reaches a maximum, and there is little, if any, increase in
blood concentrations at higher doses. Excess vitamin C is readily excreted.
As mentioned earlier, cigarette smoking increases the need for vitamin C.
Cigarette smoke contains oxidants, which greedily deplete this potent antioxidant.
Exposure to cigarette smoke, especially when accompanied by low dietary
intakes of vitamin C, depletes the body's vitamin C in both active and passive
smokers. People who chew tobacco also have low levels of vitamin C. Because
people who smoke cigarettes regularly suffer significant oxidative stress,
their requirement for vitamin C is increased an additional 35 milligrams; nonsmokers
regularly exposed to cigarette smoke should also be sure to meet their
RDA for vitamin C. Smokers are among those most likely to suffer vitamin C
deficiency.
Vitamin A was the first fat-soluble vitamin to be recognized. More than a century
later, vitamin A and its precursor, beta-carotene, continue to intrigue researchers
with their diverse roles and profound effects on health.
Three different forms of vitamin A are active in the body: retinol, retinal,
and retinoic acid. Collectively known as retinoids, these compounds are commonly
found in foods derived from animals. Foods derived from plants provide
carotenoids, some of which can be converted to vitamin A.1 * The most studied of
the carotenoids with vitamin A activity is beta-carotene, which can be split to form
retinol in the intestine and liver.2 Figure 11-1 illustrates the structural similarities
and differences of these vitamin A compounds and the cleavage of beta-carotene.
The cells can convert retinol and retinal to the other active forms of vitamin A
as needed. The conversion of retinol to retinal is reversible, but the further conversion
of retinal to retinoic acid is irreversible (see Figure 11-2). This irreversibility
is significant because each form of vitamin A performs a specific function that
the others cannot.
Several proteins participate in the digestion and absorption of vitamin A. After
absorption via the lymph system, vitamin A eventually arrives at the liver, where
it is stored. There, a special transport protein, retinol-binding protein (RBP),
picks up vitamin A from the liver and carries it in the blood. Cells that use vitamin
A have special protein receptors for it, and its action within each cell may differ
depending on the receptor. For example, retinoic acid can stimulate cell growth
in the skin and inhibit cell growth in tumors.
Roles in the Body Vitamin A is a versatile vitamin, known to regulate the
expression of several hundred genes. Its major roles include:
● Promoting vision
● Participating in protein synthesis and cell differentiation, thereby maintaining
the health of epithelial tissues and skin
● Supporting reproduction and regulating growth
As mentioned, each form of vitamin A performs specific tasks. Retinol supports
reproduction and is the major transport and storage form of the vitamin.
Retinal is active in vision and is also an intermediate in the conversion of retinol
to retinoic acid (review Figure 11-2). Retinoic acid acts like a hormone, regulating
cell differentiation, growth, and embryonic development. Animals raised on retinoic
acid as their only source of vitamin A can grow normally, but they become
blind because retinoic acid cannot be converted to retinal (review Figure 11-2).
Vitamin A in Vision Vitamin A plays two indispensable roles in the eye: it helps
maintain a crystal-clear outer window, the cornea, and it participates in the
conversion of light energy into nerve impulses at the retina (see Figure 11-3 for
details). Some of the photosensitive cells of the retina contain pigment molecules
called rhodopsin. Each rhodopsin molecule is composed of a protein
called opsin bonded to a molecule of retinal, which plays a central role in vision.
3 When light passes through the cornea of the eye and strikes the retina,
rhodopsin responds. As it does, opsin is released and retinal shifts from a cis to
a trans configuration, just as fatty acids do during hydrogenation (see p. 139).
These changes generate an electrical impulse that conveys the message to the
brain. Much of the retinal is then converted back to its active cis form and combined
with the opsin protein to regenerate rhodopsin. Some retinal, however,
may be oxidized to retinoic acid, a biochemical dead end for the visual process.
Visual activity leads to repeated small losses of retinal, necessitating its constant
replenishment either directly from foods or indirectly from retinol stores.
Vitamin A in Protein Synthesis and Cell Differentiation Despite its important role
in vision, only one-thousandth of the body's vitamin A is in the retina. Much
more is in the cells lining the body's surfaces. There, the vitamin participates in
protein synthesis and cell differentiation, a process by which each type of cell
develops to perform a specific function. All body surfaces, both inside and out, are covered by layers of cells known as
epithelial cells. The epithelial tissue on the outside of the body is, of course, the
skin—and vitamin A and beta-carotene help to protect against skin damage from
sunlight.4 The epithelial tissues that line the inside of the body are the mucous
membranes: the linings of the mouth, stomach, and intestines; the linings of
the lungs and the passages leading to them; the linings of the urinary bladder
and urethra; the linings of the uterus and vagina; and the linings of the eyelids
and sinus passageways. Within the body, the mucous membranes of the GI tract
alone line an area larger than a quarter of a football field, and vitamin A helps to
maintain their integrity (see Figure 11-4).
Vitamin A promotes differentiation of epithelial cells and goblet cells, onecelled
glands that synthesize and secrete mucus. Mucus coats and protects the
epithelial cells from invasive microorganisms and other potentially damaging
substances, such as gastric juices.
Vitamin A in Reproduction and Growth As mentioned, vitamin A also supports
reproduction and regulates growth.5 In men, retinol participates in sperm development,
and in women, vitamin A supports normal fetal development during
pregnancy. Children lacking vitamin A fail to grow; given vitamin A supplements,
these children gain weight and grow taller.
The growth of bones illustrates that growth is a complex phenomenon of
remodeling. To convert a small bone into a large bone, some bone cells must
"undo" parts of the bone before other cells can build new bone, and vitamin A
participates in the dismantling.* The cells that break down bone contain acid and
enzymes that dissolve the minerals and digest the matrix.** With the help of vitamin
A, these bone-dismantling cells destroy selected sites in the bone, removing
the parts that are not needed. After completing their work, the bone-dismantling
cells die, leaving their excavation site to be rebuilt by the bone-building cells.
Beta-Carotene as a Precursor and an Antioxidant Beta-carotene plays two primary
roles in the body.6 First, it serves as a vitamin A precursor. Second, some
beta-carotene acts as an antioxidant capable of protecting the body against disease.
Just as a deficiency of vitamin A affects all body systems,
so does a toxicity. Symptoms of toxicity begin to develop when all the binding
proteins are loaded, and vitamin A is free to damage cells. Such effects are unlikely
when a person depends on a balanced diet for nutrients, but toxicity is a
real possibility when concentrated amounts of preformed vitamin A in foods
derived from animals, fortified foods, or supplements are consumed. Children are most vulnerable to toxicity because they need less vitamin A and are more
sensitive to overdoses. An Upper Level (UL) has been set for preformed vitamin
A (see inside front cover). Even multivitamin supplements typically provide
1500 micrograms—much more vitamin A than most people need. (For
perspective, the RDA for vitamin A is 700 micrograms for women and
900 micrograms for men.)
Beta-carotene, which is found in a wide variety of fruits and vegetables, is not
converted efficiently enough in the body to cause vitamin A toxicity; instead,
it is stored in the fat just under the skin. Although overconsumption of betacarotene
from foods may turn the skin yellow, this is not harmful (see Figure 11-6).
In contrast, overconsumption of beta-carotene from supplements may be quite
harmful. In excess, this antioxidant may act as a prooxidant (as Highlight 11 explains).
Adverse effects of beta-carotene supplements are most evident in people
who drink alcohol and smoke cigarettes.
Bone Defects Excessive intakes of vitamin A over the years may weaken the
bones and contribute to fractures and osteoporosis.12 Vitamin A suppresses bonebuilding
activity, stimulates bone-dismantling activity, and interferes with vitamin
D's ability to maintain normal blood calcium.
Birth Defects Excessive vitamin A during pregnancy leads to abnormal cell
death in the spinal cord, which increases the risk of birth defects such as spina
bifida and cleft palate.13 In such cases, vitamin A is considered a teratogen.
High intakes (daily supplemental intakes of vitamin A equivalent to roughly
four times the RDA for women) before the seventh week of pregnancy appear
to be the most damaging. For this reason, vitamin A is not given as a supplement
in the first trimester of pregnancy without specific evidence of deficiency,
which is rare.
Not for Acne Adolescents need to know that massive doses of vitamin A have no
beneficial effect on acne. The prescription medicine Accutane is made from vitamin
A but is chemically different.* Taken orally, Accutane is effective against the
deep lesions of cystic acne. It is highly toxic, however, especially during growth,
and has caused birth defects in infants when women have taken it during their
pregnancies. For this reason, women taking Accutane must agree to pregnancy
testing and to using two forms of contraception from at least 1 month before
taking the drug through at least 1 month after discontinuing its use. Should they
become pregnant, they need to stop taking Accutane immediately and notify
their physician.
Another vitamin A relative, Retin-A, fights acne, the wrinkles of aging, and
other skin disorders.** Applied topically, this ointment smooths and softens
skin; it also lightens skin that has become darkly pigmented after inflammation.
During treatment, the skin becomes red and tender and peels.
The richest sources of the retinoids are foods derived
from animals—liver, fish liver oils, milk and milk products, butter, and eggs. Because
vitamin A is fat soluble, it is lost when milk is skimmed. To compensate,
reduced-fat, low-fat, and fat-free milks are fortified so as to provide the amount
found in whole milk. Margarine is usually fortified to provide the same amount
of vitamin A as butter.
Plants contain no retinoids, but many vegetables and some fruits contain
vitamin A precursors—the carotenoids. Only a few carotenoids have vitamin
A activity; the carotenoid with the greatest vitamin A activity is betacarotene.
Beta-carotene is a rich, deep yellow, almost orange, compound.
The beta-carotene in dark green, leafy vegetables is abundant, but masked
by large amounts of the green pigment chlorophyll. Attractive meals that include
colorful fruits and vegetables rich in beta-carotene are likely to provide
vitamin A.14
The Colors of Vitamin A Foods Dark leafy greens (like broccoli and spinach—not
celery or cabbage) and rich yellow or deep orange vegetables and fruits (such as
cantaloupe, carrots, and sweet potatoes—not corn or bananas) help people meet
their vitamin A needs (see Figure 11-7 on p. 350). A diet including several servings
of such carotene-rich sources helps to ensure a sufficient intake.
Bright color is not always a sign of vitamin A activity, however. Beets and
corn, for example, derive their colors from the red and yellow xanthophylls,
which have no vitamin A activity. As for white plant foods such as potatoes,
cauliflower, pasta, and rice, they also offer little or no vitamin A. Similarly, fast
foods often lack vitamin A. Anyone who dines frequently on hamburgers, french
fries, and colas is wise to emphasize colorful vegetables and fruits at other meals. Vitamin A-Rich Liver People sometimes wonder if eating liver too frequently
can cause vitamin A toxicity. Liver is a rich source because vitamin A is stored
in the livers of animals, just as in humans.* Arctic explorers who have eaten
large quantities of polar bear liver have become ill with symptoms suggesting
vitamin A toxicity. Liver offers many nutrients, and eating it periodically
may improve a person's nutrition status, but caution is warranted not to eat
too much too often, especially for pregnant women. With 1 ounce of beef
liver providing more than three times the RDA for vitamin A, intakes can rise
quickly.
Golden Rice As mentioned earlier, vitamin A deficiency is a major problem in
developing countries, impairing growth, causing blindness, and suppressing
the immune system. In these developing regions of the world, fruits and vegetables
are a scarcity, and rice, which contains no beta-carotene or vitamin A,
is the staple food. Through biotechnology, scientists have been able to genetically
modify rice to be a significant source of beta-carotene. Commonly
called golden rice because of its yellowish tinge, this rice offers a promising solution
to world malnutrition, but it also raises questions about the potential
risks to the environment. More details are provided in Highlight 19's review
of food biotechnology and Chapter 20's presentation of world hunger and
possible solutions.
Though called a vitamin, the active form of vitamin D
is actually a hormone—a compound manufactured by one part of the body that travels through the blood and causes another body part to respond. Like vitamin
A, vitamin D has a binding protein that carries it to the target organs—most
notably, the intestines, the kidneys, and the bones. All respond to vitamin D by
making the minerals needed for bone growth and maintenance available.
Vitamin D in Bone Growth Vitamin D is a member of a large and cooperative
bone-making and maintenance team composed of nutrients and other compounds,
including vitamins A and K; the hormones parathyroid hormone and
calcitonin; the protein collagen; and the minerals calcium, phosphorus, magnesium,
and fluoride. Vitamin D's special role in bone health is to assist in the
absorption of calcium and phosphorus, thus helping to maintain blood concentrations
of these minerals. The bones grow denser and stronger as they absorb
and deposit these minerals. Details of calcium balance and mineral deposition
appear in Chapter 12, but here's a sneak preview: adequate nutrition and regular
exercise are essential to achieving peak bone mass before age 30.
Vitamin D raises blood concentrations of bone minerals in three ways. When
the diet is sufficient, vitamin D enhances mineral absorption from the GI tract.
When the diet is insufficient, vitamin D provides the needed minerals from other
sources: reabsorption by the kidneys and mobilization from the bones into the
blood. The vitamin may work alone, as it does in the GI tract, or in combination
with parathyroid hormone, as it does in the bones and kidneys.
Vitamin D in Other Roles Scientists have discovered many other tissues that
respond to vitamin D, as the following examples describe. In the brain and nerve
cells, vitamin D protects against cognitive decline and slows the progression of
Parkinson disease.16 Vitamin D in muscle cells encourages growth in children
and preserves strength in adults.17 Vitamin D signals cells of the immune system
to defend against infectious diseases.18 Vitamin D may also regulate the cells of
the adipose tissue in ways that might influence the development of obesity. In many cases, vitamin D enhances or suppresses the activity of genes that
regulate cell growth. As such, it may be valuable in treating a number of diseases.
Recent research suggests that vitamin D may protect against metabolic syndrome,
type 2 diabetes, tuberculosis, inflammation, multiple sclerosis, macular degeneration,
hypertension, and some cancers.20 Even so, evidence does not support
vitamin D supplementation to improve health beyond correcting deficiencies.21
In fact, some evidence suggests certain cancers are associated with both too little
and too much vitamin D, making routine supplementation potentially harmful.
Chapter 7 describes how the body's cells use oxygen in metabolic reactions.
In the process, oxygen reacts with body compounds and produces
highly unstable molecules known as free radicals. In addition
to normal body processes, environmental factors such as ultraviolet
radiation, air pollution, and tobacco smoke generate free radicals.
A free radical is a molecule with one or more unpaired electrons.*
An electron without a partner is unstable and highly reactive. To regain
its stability, the free radical quickly finds a stable but vulnerable
compound from which to steal an electron.
With the loss of an electron, the formerly stable molecule becomes
a free radical itself and steals an electron from another nearby molecule.
Thus an electron-snatching chain reaction is under way with
free radicals producing more free radicals. Antioxidants neutralize
free radicals by donating one of their own electrons, thus ending the chain reaction. When they lose electrons, antioxidants do not become
free radicals because they are stable in either form. (Review
Figure 10-16 on p. 328 to see how ascorbic acid can give up two hydrogens
with their electrons and become dehydroascorbic acid.)
Free radicals attack. Occasionally, these free-radical attacks are
helpful. For example, cells of the immune system use free radicals as
ammunition in an "oxidative burst" that demolishes disease-causing
viruses and bacteria. Most often, however, free-radical attacks cause
widespread damage. They commonly damage the polyunsaturated
fatty acids in lipoproteins and in cell membranes, disrupting the transport
of substances into and out of cells. Free radicals also alter DNA,
RNA, and proteins, creating excesses and deficiencies of specific proteins,
impairing cell functions, and eliciting an inflammatory response.
All of these actions contribute to cell damage, disease progression,
and aging (see Figure H11-1).
The body's natural defenses and repair systems try to control the
destruction caused by free radicals, but these systems are not 100
percent effective. In fact, they become less effective with age, and
the unrepaired damage accumulates. To some extent, dietary antioxidants
defend the body against oxidative stress, but if antioxidants
are unavailable or if free-radical production becomes excessive, health
problems may develop.1 Oxygen-derived free radicals may cause diseases,
not only by indiscriminately destroying the valuable components of cells, but also by serving as signals for specific activities within the
cells. Scientists have identified oxidative stress as a causative factor
and antioxidants as a protective factor in cognitive performance and
the aging process as well as in the development of diseases such as
cancer, arthritis, cataracts, diabetes, hypertension, and heart disease.2
Defending against Free Radicals
The body maintains a couple lines of defense against free-radical
damage. A system of enzymes disarms the most harmful oxidants.*
The action of these enzymes depends on the minerals selenium, copper,
manganese, and zinc. If the diet fails to provide adequate supplies
of these minerals, this line of defense weakens. The body also uses
the antioxidant vitamins—vitamin E, beta-carotene, and vitamin C.
Vitamin E defends the body's lipids (cell membranes, nervous tissues,
and lipoproteins, for example) by efficiently stopping the free-radical
chain reaction.3 Beta-carotene also acts as an antioxidant in lipid
membranes. Vi tamin C protects other tissues, such as the skin and
fluid of the blood, against free-radical attacks. Vitamin C seems especially
adept at neutralizing free radicals from polluted air and cigarette
smoke; it also restores oxidized vitamin E to its active state.
Dietary antioxidants also include some of the phytochemicals (featured
in Highlight 13). Together, nutrients and phytochemicals with antioxidant
activity minimize damage and prevent disease in the following ways: 4
● Limiting free-radical formation
● Destroying free radicals or their precursors
● Stimulating antioxidant enzyme activity
● Repairing oxidative damage
● Stimulating repair enzyme activity
● Supporting a healthy immune system
These actions play key roles in defending the body
against chronic diseases such as cancer and heart
disease. Defending against Cancer
Cancers arise when cellular DNA is damaged—
sometimes by free-radical attacks. Antioxidants
may reduce cancer risks by protecting DNA from this
damage. Many researchers have reported low rates
of cancer in people whose diets include abundant
vegetables and fruits, rich in antioxidants. Preliminary
reports suggest an inverse relationship between
DNA damage and vegetable intake and a positive relationship
with beef and pork intake.5
Foods rich in vitamin C seem to protect against certain
types of cancers, especially those of the esophagus.
Such a correlation may reflect the benefits of a diet rich
in fruits and vegetables and low in fat; evidence that vitamin
C supplements reduce the risk of cancer is lacking.
Researchers hypothesize that vitamin E might inhibit cancer formation
by attacking free radicals that damage DNA. Evidence that vitamin
E supplements help guard against cancer, however, is lacking.
Several studies report a cancer-preventing benefit of vegetables
and fruits rich in beta-carotene and the other carotenoids as
well. Carotenoids may protect against oxidative damage to DNA.
Some research suggests that high concentrations of beta-carotene
and the other carotenoids are associated with lower rates of some
cancers.6 Studies do not, however, find a reduction in cancer risk
with beta-carotene supplementation. Benefits most likely reflect
a healthy diet abundant in fruits and vegetables. In fact, a major
review of several large research studies concluded that none produced
evidence to justify the use of antioxidant supplements for
cancer prevention.7
Defending against Heart Disease
Decades of research have contributed to our understanding of how oxidative
stress contributes to atherosclerosis and how antioxidants might
protect against heart disease, yet questions remain.8 High blood cholesterol
carried in LDL (low-density lipoproteins) is a major risk factor for
cardiovascular disease, but how do LDL exert their damage? One scenario
is that free radicals within the arterial walls oxidize LDL, changing
their structure and function. The oxidized LDL then accelerate the formation
of artery-clogging plaques. These free radicals also oxidize the
polyunsaturated fatty acids of the cell membranes, sparking additional
changes in the arterial walls, which impede the flow of blood. Susceptibility
to such oxidative damage within the arterial walls is heightened
by a diet high in saturated fat and by cigarette smoke. In contrast, diets that include plenty of fruits and vegetables, especially when saturated
fat is low, strengthen antioxidant defenses against LDL oxidation.
Antioxidants, especially vitamin E, may protect against hypertension
and cardiovascular disease.9 Epidemiological studies suggest that
people who eat foods rich in vitamin E have relatively few atherosclerotic
plaques and low rates of death from heart disease. Among
its many protective roles, vitamin E defends against LDL oxidation,
inflammation, arterial injuries, and blood clotting. Whether vitamin E
supplements slow the progression of heart disease is less clear.
Some studies suggest that vitamin C protects against LDL oxidation,
raises HDL, lowers total cholesterol, and improves blood pressure.
Vitamin C may also minimize inflammation and the free-radical
action within the arterial wall. Like vitamin E, the role of vitamin C
supplements in reducing the risk of heart disease remains uncertain.
In the process of scavenging and quenching free radicals, antioxidants
themselves become oxidized. To some extent, they can be regenerated,
but losses still occur and free radicals attack continuously. To maintain
defenses, a person must replenish dietary antioxidants regularly. But
should antioxidants be replenished from foods or from supplements?
Foods—especially fruits and vegetables—offer not only antioxidants,
but an array of other valuable vitamins and minerals as well.
Importantly, deficiencies of these nutrients can damage DNA as readily
as free radicals can. Eating fruits and vegetables in abundance
protects against both deficiencies and diseases—and may protect
against inflammation and DNA damage.10 A major review of the evidence
gathered from metabolic studies, epidemiologic studies, and
dietary intervention trials identified three dietary strategies most effective
in preventing heart disease:
● Use unsaturated fats instead of saturated or trans fats (see Highlight
5).
● Select foods rich in omega-3 fatty acids (see Chapter 5).
● Consume a diet high in fruits, vegetables, nuts, and whole grains
and low in refined grain products.
Such a diet combined with exercise, weight control, and not smoking
serves as the best prescription for health. Notably, taking supplements
is not among these disease-prevention recommendations.
Diets that deliver sufficient quantities of antioxidant vitamins may
protect against cancer and heart disease—but only a small fraction
of the US population consumes recommended amounts. Some
research suggests a protective effect from as little as a daily glass
of orange juice or carrot juice (rich sources of vitamin C and betacarotene,
respectively). Other intervention studies, however, have
used levels of nutrients that far exceed current recommendations and
can be achieved only by taking supplements. In making their recommendations
for the antioxidant nutrients, members of the DRI Committee
considered whether these studies support substantially higher
intakes to help protect against chronic diseases. They did raise the
recommendations for vitamins C and E, but they do not support taking
supplements over eating a healthy diet. Though fruits and vegetables containing many antioxidant nutrients
and phytochemicals have been associated with a diminished risk of
many chronic diseases, supplements have not always proved beneficial.
11 In fact, sometimes the benefits are more apparent when the vitamins
come from foods rather than from supplements. In other words,
the antioxidant actions of fruits and vegetables are greater than their
nutrients alone can explain. Without data to confirm the benefits of supplements,
we cannot accept the potential risks. And the risks are real.
Consider the findings from a meta-analysis of the relationships between
supplements of vitamin A, vitamin E, beta-carotene, or combinations
and total mortality. Researchers concluded that supplements
provided no benefits and actually increased mortality.12 Beta-carotene
increases the risk of lung cancer and overall mortality in smokers.13
A large research study on cancer prevention was prematurely terminated
when researchers noted a trend toward developing diabetes
in subjects receiving selenium and a slight increased risk of prostate
cancer in those receiving vitamin E.14 Another study concluded that
vitamin E supplements increase the risk of some strokes, but reduce
the risk of others, making its indiscriminate use unwise.15
Even if research clearly proves that a particular nutrient is the ultimate
protective ingredient in foods, supplements would not be the answer
because their contents are limited. Vitamin E supplements, for example,
usually contain alpha-tocopherol, but foods provide an assortment of tocopherols
and tocotrienols among other nutrients, many of which provide
valuable protection against free-radical damage. In addition to a full array
of nutrients, foods provide phytochemicals that also fight against many diseases. Supplements shortchange users. Furthermore, supplements
should be used only as an adjunct to other measures such as smoking cessation,
weight control, physical activity, and medication as needed.
Clearly, much more research is needed to define optimal and harmful
levels of intake. This much we know: antioxidants behave differently
under various conditions. At physiological levels typical of a healthy
diet, they act as antioxidants, but at pharmacological doses typical of
supplements, they may act as prooxidants, stimulating the production
of free radicals and altering metabolism in a way that may promote
disease. A high intake of vitamin C from supplements, for example, may
increase the risk of heart disease in women with diabetes. Until the
optimum intake of antioxidant nutrients can be determined, the risks
of supplement use remain unclear. Table H11-1 presents a summary of
the relationships between antioxidants and chronic diseases—sorted
by foods or supplements. As you can see, many studies report either
no effect or inconsistent results. Any decrease in risk is attributed to foods 9 out of 10 times. Any increase in risk is always from supplements,
and often in smokers. Clearly, the best way to add antioxidants
to the diet is to eat generous servings of fruits and vegetables daily.
It should be clear by now that we cannot know the identity and
action of every chemical in every food. Even if we did, why create
a supplement to replicate a food? Why not eat foods and enjoy the
pleasure, nourishment, and health benefits they provide? The beneficial
constituents in foods are widespread among plants. Among the
fruits, pomegranates, berries, and citrus rank high in antioxidants; top
antioxidant vegetables include kale, spinach, and brussels sprouts;
millet and oats contain the most antioxidants among the grains; pinto
beans and soybeans are outstanding legumes; and walnuts outshine
the other nuts. But don't try to single out one particular food for its
"magical" nutrient, antioxidant, or phytochemical. Instead, eat a wide
variety of fruits, vegetables, grains, legumes, and nuts every day—
and get all the benefits these foods have to offer.
Water constitutes about 60 percent of an adult's body weight and a higher percentage
of a child's (see Figure 1-1, p. 7). Because water makes up about 75 percent
of the weight of lean tissue and less than 25 percent of the weight of fat, a
person's body composition influences how much of the body's weight is water.
The proportion of water is generally smaller in females, obese people, and the
elderly because of their smaller proportion of lean tissue.
In the body, water is the fluid in which all life processes occur. The water in
the body fluids:
● Carries nutrients and waste products throughout the body
● Maintains the structure of large molecules such as proteins and glycogen
● Participates in metabolic reactions
● Serves as the solvent for minerals, vitamins, amino acids, glucose, and many
other small molecules so that they can participate in metabolic activities
● Acts as a lubricant and cushion around joints and inside the eyes, the spinal
cord, and, in pregnancy, the amniotic sac surrounding the fetus in the womb
● Aids in the regulation of normal body temperature, as the evaporation of
sweat from the skin removes excess heat from the body
● Maintains blood volume
To support these and other vital functions, the body actively maintains an
appropriate water balance between intake and output.
Water Balance and Recommended Intakes Every cell contains fluid of
the exact composition that is best for that cell. Fluid inside cells is called intracellular
fluid, whereas fluid outside cells is called extracellular fluid. The extracellular
fluid that surrounds each cell is called interstitial fluid, whereas the extracellular
fluid in the blood vessels is called intravascular fluid. Figure 12-1 illustrates a cell
and its associated fluids. The compositions of intercellular and extracellular fluids
differ from each other. They continuously lose and replace their components, yet
the composition in each compartment remains remarkably constant under normal
conditions. Because imbalances can be devastating, the body quickly responds by
adjusting both water intake and excretion as needed. Consequently, the entire system
of cells and fluids remains in a delicate, but controlled, state of homeostasis.
Water Intake Thirst and satiety influence water intake in response to changes
sensed by the mouth, hypothalamus, and nerves. When water intake is inadequate,
the blood becomes concentrated (having lost water but not the dissolved
substances within it), the mouth becomes dry, and the hypothalamus initiates
drinking behavior. When water intake is excessive, the stomach expands and
stretch receptors send signals to stop drinking. Similar signals are sent from receptors
in the heart as blood volume increases.
When too much water is lost from the body and not replaced, dehydration develops.
A first sign of dehydration is thirst, the signal that the body has lost some
fluid. If a person is unable to obtain water or, as in many elderly people, fails to perceive
the thirst message, the symptoms of dehydration may progress rapidly from
thirst to weakness, exhaustion, and delirium—and end in death if not corrected (see
Table 12-1). Notice that an early sign of dehydration is fatigue; keep that in mind
when considering caffeinated beverages for an afternoon "pick-me-up" and choose
water instead. Dehydration develops with either inadequate water intake or excessive
water losses. (Chapter 14 revisits dehydration and the fluid needs of athletes.)
Water intoxication, on the other hand, is rare but can occur with excessive water
intake and kidney disorders that reduce urine production. The symptoms may
include confusion, convulsions, and even death in extreme cases. Excessive water
ingestion (10 to 20 liters) within a few hours dilutes the sodium concentration
of the blood and contributes to a dangerous condition known as hyponatremia. For this reason, guidelines suggest limiting fluid intake during times of heavy
sweating to between 1 and 1.5 liters per hour. (Chapter 14 revisits hyponatremia
as sometimes seen in endurance athletes.)
Water Sources The obvious dietary source of water is water itself, which provides
about one-third of the total water intake in the United States.1 In addition,
other beverages and nearly all foods also contain water. Most fruits and vegetables
contain up to 90 percent water, and many meats and cheeses contain at least
50 percent. See Table 12-2 for selected foods and Appendix H for many more. Also,
metabolic water is generated as an end product during condensation reactions
and the oxidation of energy-yielding nutrients. Recall from Chapter 7 that when
the energy-yielding nutrients break down, their carbons and hydrogens combine
with oxygen to yield carbon dioxide (CO2) and water (H2O). As Table 12-3 shows,
the water derived daily from these three sources—beverages, foods, and metabolism—
averages about 2500 milliliters (roughly 2.5 quarts or 10.5 cups).
Water Losses At the very least, the body must excrete enough water to carry
away the waste products generated by a day's metabolic activities. This obligatory
water excretion is a minimum of about 500 milliliters (about 2 cups) of
water each day. Above this amount, excretion adjusts to balance intake. If a person
drinks more water, the kidneys excrete more urine, and the urine becomes
more dilute. In addition to urine, water is lost from the lungs as vapor and from
the skin as sweat; some is also lost in feces.* The amount of fluid lost from each
source varies, depending on the environment (such as heat or humidity) and the
body's physical condition (such as exercise or fever). On average, daily losses total
about 2500 milliliters. Table 12-3 shows how daily water losses and intakes
balance; maintaining this balance requires healthy kidneys and an adequate intake
of fluids. An adequate intake of fluids, in turn, helps to maintain healthy
kidneys and prevent kidney stone formation.2
Water Recommendations Because water needs vary depending on diet, activity,
environmental temperature, and humidity, a general water requirement is difficult
to establish. Recommendations are sometimes expressed in proportion to
the amount of energy expended under average environmental conditions; for adults, for example, 1.0 to 1.5 milliliters per kcalorie expended (roughly one-half
cup per 100 kcalories). The recommended water intake for a person who expends
2000 kcalories a day, then, is 2 to 3 liters of water (about 8 to 12 cups). This recommendation
is in line with the Adequate Intake (AI) for total water set by the
DRI Committee. Total water includes not only drinking water, but water in other
beverages and in foods as well. Only one in five adults in the United States report
drinking at least 8 cups of water a day.3
Because a wide range of water intakes will prevent dehydration and its harmful
consequences, the AI is based on average intakes. People who are physically
active or who live in hot environments may need more.
Which beverages are best? Any beverage can readily meet the body's f luid
needs, but those with few or no kcalories do so without contributing to weight
gain. Given that obesity is a major health problem and that beverages currently
represent more than 20 percent of the total energy intake in the United States,
water is the best choice for most people. Other choices include tea, coffee, nonfat
and low-fat milk and soymilk, artificially sweetened beverages, fruit and vegetable
juices, sports drinks, and lastly, sweetened nutrient-poor beverages.
Some research indicates that people who drink caffeinated beverages lose a
little more fluid than when drinking water because caffeine acts as a diuretic. The
DRI Committee considered such findings in their recommendations for water intake
and concluded that caffeinated beverages contribute to the daily total water
intake similar to that contributed by non-caffeinated beverages. In other words,
it doesn't seem to matter whether people rely on caffeine-containing beverages or
other beverages to meet their fluid needs.
As Highlight 7 explains, alcohol acts as a diuretic and can impair a person's
health. Alcohol should not be used to meet fluid needs.
Health Effects of Water Water supports good health.4 Physical and mental performances
depend on it, as does the optimal functioning of the GI tract, kidneys,
heart, and other body systems.
The kind of water a person drinks may also make a difference to health. Water
is usually either hard or soft. Hard water has high concentrations of calcium and
magnesium; the principal mineral of soft water is sodium or potassium. (See the
accompanying glossary for other common terms used to describe water.) In practical
terms, soft water makes more bubbles with less soap; hard water leaves a ring on
the tub, a crust of rocklike crystals in the teakettle, and a gray residue in the laundry.
Soft water may seem more desirable around the house, and some homeowners
purchase water softeners that replace magnesium and calcium with sodium. In
the body, however, soft water with sodium may aggravate hypertension and heart
disease. In contrast, the minerals in hard water may benefit these conditions.
Soft water also more easily dissolves certain contaminant minerals, such as
cadmium and lead, from old plumbing pipes. As Chapter 13 explains, these contaminant
minerals harm the body by displacing the nutrient minerals from their
normal sites of action. People who live in buildings with old plumbing should
run the cold water tap a minute or two to flush out harmful minerals whenever
the water faucet has been off for more than 6 hours.5
Many people select bottled water, believing it to be safer than tap water and
therefore worth its substantial cost. Chapter 19 offers a discussion of bottled water
safety and regulations.
Blood Volume and Blood Pressure Fluids maintain the blood volume,
which in turn influences blood pressure. The kidneys are central to the regulation
of blood volume and blood pressure. All day, every day, the kidneys reabsorb
needed substances and water and excrete wastes with some water in the urine
(see Figure 12-2). The kidneys meticulously adjust the volume and the concentration
of the urine to accommodate changes in the body, including variations in
the day's food and beverage intakes. Instructions on whether to retain or release
substances or water come from ADH, renin, angiotensin, and aldosterone. ADH Whenever blood volume or blood pressure falls too low, or whenever the
extracellular fluid becomes too concentrated, the hypothalamus signals the pituitary
gland to release antidiuretic hormone (ADH). ADH is a water-conserving
hormone that stimulates the kidneys to reabsorb water. Consequently, the
more water you need, the less your kidneys excrete. These events also trigger
thirst. Drinking water and retaining fluids raise the blood volume and dilute
the concentrated fluids, thus helping to restore homeostasis. (Recall from Highlight
7 that alcohol depresses ADH activity, thus promoting fluid losses and
dehydration.)
Renin Cells in the kidneys respond to low blood pressure by releasing an enzyme
called renin. Through a complex series of events, renin causes the kidneys
to reabsorb sodium. Sodium reabsorption, in turn, is always accompanied by
water retention, which helps to raise blood volume and blood pressure. Angiotensin In addition to its role in sodium retention, renin hydrolyzes a
protein from the liver called angiotensinogen to angiotensin I. Angiotensin I
is inactive until another enzyme converts it to its active form—angiotensin II.
Angiotensin II is a powerful vasoconstrictor that narrows the diameters of blood
vessels, thereby raising the blood pressure.
Aldosterone In addition to acting as a vasoconstrictor, angiotensin II stimulates
the release of the hormone aldosterone from the adrenal glands. Aldosterone
signals the kidneys to excrete potassium and to retain more sodium, and therefore
water, because when sodium moves, water follows. Again, the effect is that
when more water is needed, less is excreted.
All of these actions are presented in Figure 12-3 and help to explain why highsodium
diets aggravate conditions such as hypertension and edema. Too much
sodium causes water retention and an accompanying rise in blood pressure or
swelling in the interstitial spaces. Chapter 18 discusses hypertension in detail.
Fluid and Electrolyte Balance Maintaining a balance of about two-thirds
of the body fluids inside the cells and one-third outside is vital to the life of the
cells. If too much water were to enter the cells, they might rupture; if too much
water were to leave, they would collapse. To control the movement of water, the cells direct the movement of the major minerals—sodium, chloride, potassium,
calcium, phosphorus, magnesium, and sulfur. Dissociation of Salt in Water When a mineral salt such as sodium chloride
(NaCl) dissolves in water, it separates (dissociates) into ions—positively and
negatively charged particles (Na+ and Cl-). The positive ions are cations; the negative
ones are anions. (To remember the difference between cations and anions,
think of the "t" in cations as a "plus" sign and the "n" in anions as a "negative.")
Unlike pure water, which conducts electricity poorly, ions dissolved in water
carry electrical current. For this reason, salts that dissociate into ions are called
electrolytes, and fluids that contain them are electrolyte solutions.
In all electrolyte solutions, anion and cation concentrations are balanced (the
number of negative and positive charges are equal). If a fluid contains 1000 negative
charges, it must contain 1000 positive charges too. If an anion enters the
fluid, a cation must accompany it or another anion must leave so that electrical
neutrality will be maintained. Thus, whenever sodium (Na+) ions leave a cell, potassium
(K+) ions enter, for example. In fact, it's a good bet that whenever Na+ and
K+ ions are moving, they are going in opposite directions.
Table 12-4 shows that, indeed, the positive and negative charges inside and
outside cells are perfectly balanced even though the numbers of each kind of
ion differ over a wide range. Inside the cells, the positive charges total 202 and
the negative charges balance these perfectly. Outside the cells, the amounts and
proportions of the ions differ from those inside, but again the positive and negative
charges balance. Scientists count these charges in milliequivalents per liter
(mEq/L).
Electrolytes Attract Water Electrolytes attract water. Each water molecule has
a net charge of zero, but the oxygen side of the molecule has a slight negative
charge, and the hydrogens have a slight positive charge. Figure 12-4 (p. 378)
shows the result in an electrolyte solution: both positive and negative ions attract
clusters of water molecules around them. This attraction dissolves salts in water
and enables the body to move fluids into appropriate compartments.
Water Follows Electrolytes As Figure 12-5 (p. 378) shows, some electrolytes reside
primarily outside the cells (notably, sodium, chloride, and calcium), whereas
others reside predominantly inside the cells (notably, potassium, magnesium, phosphate, and sulfate). Cell membranes are selectively permeable,
meaning that they allow the passage of some molecules, but not
others. Whenever electrolytes move across the membrane, water
follows.
The movement of water across a membrane toward the more
concentrated solutes is called osmosis. The amount of pressure
needed to prevent the movement of water across a membrane is
called the osmotic pressure. Figure 12-6 presents osmosis, and
the photos of salted eggplant and rehydrated raisins provide familiar
examples.
Proteins Regulate Flow of Fluids and Ions Chapter 6 describes
how proteins attract water and help to regulate fluid movement.
It explains that when proteins leak out of the blood vessels into
the spaces between the cells, fluids follow and cause the swelling
of edema. In addition, transport proteins in the cell membranes
regulate the passage of positive ions and other substances
from one side of the membrane to the other. Negative ions follow
positive ions, and water flows toward the more concentrated
solution.
An example of a protein that regulates the flow of fluids and
ions in and out of cells is the sodium-potassium pump. The
pump actively exchanges sodium for potassium across the cell
membrane, using ATP as an energy source. Figure 6-10 on p. 181
illustrates this action. Regulation of Fluid and Electrolyte Balance The amounts of various
minerals in the body must remain nearly constant. Regulation
occurs chiefly at two sites: the GI tract and the kidneys.
Minerals in foods enter the body by way of the GI tract. In addition, the digestive
juices of the GI tract contain minerals. These minerals and those from foods
are absorbed in the large intestine or excreted as needed. Each day, 8 liters of fluids
and associated minerals are recycled this way, providing ample opportunity
for the regulation of electrolyte balance.
The kidneys' control of the body's water content by way of the hormone ADH
has already been described (see p. 375). The kidneys regulate the electrolyte contents
by responding to the hormone aldosterone (also explained on p. 376). If
the body's sodium is low, aldosterone stimulates sodium reabsorption from the kidneys. As sodium is reabsorbed, potassium
(another positive ion) is excreted in
accordance with the rule that total positive
charges must remain in balance with
total negative charges.
Fluid and Electrolyte Imbalance
Normally, the body defends itself
successfully against fluid and electrolyte
imbalances. Certain situations and some
medications, however, may overwhelm
the body's ability to compensate. Severe,
prolonged vomiting and diarrhea as well
as heavy sweating, burns, and traumatic
wounds may incur such great f luid and
electrolyte losses as to precipitate a medical
emergency.
Di f ferent Solutes Los t by Di f ferent
Routes Different solutes are lost depending
on why fluid is lost. If fluid is lost by
vomiting or diarrhea, sodium is lost indiscriminately. If the adrenal glands
oversecrete aldosterone, as may occur when they develop a tumor, the kidneys
may excrete too much potassium. A person with uncontrolled diabetes may lose
glucose, a solute not normally excreted, and large amounts of fluid with it. Each
situation results in dehydration, but drinking water alone will not restore electrolyte
balance. Medical intervention is required.
Replacing Lost Fluids and Electrolytes In many cases, people can replace the
fluids and minerals lost in sweat or in a temporary bout of diarrhea by drinking
plain cool water and eating regular foods. Some cases, however, demand rapid
replacement of fluids and electrolytes—for example, when diarrhea threatens
the life of a malnourished child. Caregivers around the world have learned to
use oral rehydration therapy (ORT)—a simple solution of sugar, salt, and water,
taken by mouth—to treat dehydration caused by diarrhea. These lifesaving
formulas do not require hospitalization and can be prepared from ingredients
available locally. Caregivers need only learn to measure ingredients carefully and
use sanitary water. Once rehydrated, a person can begin eating foods. (Chapter 14
presents a discussion of sport drinks.)
Although all the major minerals help to maintain the body's fluid balance as described
earlier, sodium, chloride, and potassium are most noted for that role. For
this reason, these three minerals are discussed first here. Later sections describe
the minerals most noted for their roles in bone growth and health—calcium,
phosphorus, and magnesium. The chapter closes with a brief discussion on sulfate,
a mineral required for the synthesis of several sulfur-containing compounds.
Sodium People have held salt (sodium chloride) in high regard throughout recorded
history. We describe someone we admire as "the salt of the earth" and
people who are not productive as "not worth their salt." The word salary comes
from the Latin word for salt, a valued commodity.
Cultures vary in their use of salt, but most people find its taste innately appealing.
Salt brings its own tangy taste and enhances other flavors, most likely
by suppressing the bitter flavors. You can taste this effect for yourself: tonic water
with its bitter quinine tastes sweeter with a little salt added. Sodium Roles in the Body Sodium is the principal cation of the extracellular fluid
and the primary regulator of its volume. Sodium also helps maintain acid-base
balance and is essential to nerve impulse transmission and muscle contraction.*
Sodium is readily absorbed by the intestinal tract and travels freely in the
blood until it reaches the kidneys, which filter all the sodium out of the blood.
Then, with great precision, the kidneys return to the blood the exact amount of
sodium the body needs. Normally, the amount excreted is approximately equal
to the amount ingested on a given day. When blood sodium rises, as when a
person eats salted foods, thirst signals the person to drink until the appropriate
sodium-to-water concentration is restored. Then the kidneys excrete both the excess
water and the excess sodium together. Both too much and too little sodium
in the diet increase the risk of heart disease.6 The key to good health, then, is
finding the balance that meets the relatively small need for this essential nutrient
but does not exceed the amount that leads to hypertension and heart disease.7
Sodium Recommendations Diets rarely lack sodium, and even when intakes are
low, the body adapts by reducing sodium losses in urine and sweat, thus making
deficiencies unlikely. Sodium recommendations are set low enough to protect
against high blood pressure, but high enough to allow an adequate intake of
other nutrients with a typical diet. Because high sodium intakes correlate with
high blood pressure, the Upper Level (UL) for adults is set at 2300 milligrams per
day, as is the Daily Value used on food labels. The average sodium intake in the
United States is 3400 milligrams, which exceeds recommendations—and most
adults will develop hypertension at some point in their lives.8
Sodium and Hypertension For years, a high sodium intake was considered the primary
factor responsible for high blood pressure. Then research pointed to salt
(sodium chloride) as the dietary culprit. Salt has a greater effect on blood pressure
than either sodium or chloride alone or in combination with other ions. The
response to a high salt meal may be immediate, reducing blood flow through
arteries; this condition is reversible if such meals are not habitual.9 The elevation
of blood pressure in response to a high-salt diet over years is progressive, and the
damage caused to blood vessels is irreversible.
Blood pressure increases in response to excesses in salt intake—most notably for
those with hypertension, African Americans, and people older than 40 years of age.
For them, a high salt intake correlates strongly with heart disease, and salt restriction
(to no more than 1500 milligrams of sodium per day) helps to lower blood pressure.
A salt-restricted diet lowers blood pressure and improves heart disease risk
in people without hypertension as well.10 Because reducing salt intake causes
no harm and diminishes the risk of hypertension and heart disease, the Dietary
Guidelines for Americans advise limiting daily salt intake to about 1 teaspoon (the
equivalent of about 2.3 grams or 2300 milligrams of sodium).11 The American
Heart Association goal is to lower blood pressure by reducing sodium intake to
less than 1500 milligrams a day.12 The "How To" feature on p. 384 offers strategies
for cutting salt (and therefore sodium) intake.
DIETARY GUIDELINES FOR AMERICANS
Choose foods low in sodium and prepare foods with little salt. Reduce daily
sodium intake to less than 2300 milligrams and further reduce intake to
1500 milligrams among persons who are 51 and older and those of any age who
are African American or have hypertension, diabetes, or chronic kidney disease.
Given the current US food supply and typical eating habits, creating a nutritionally
balanced diet that meets sodium recommendations can be quite a challenge.
13 One eating pattern, known as the DASH (Dietary Approaches to Stop
Hypertension) Eating Plan, is especially effective in lowering blood pressure Like other USDA Food Patterns, the DASH Eating Plan reflects the Dietary Guidelines
and allows people to stay within their energy allowance, meet nutrient needs,
and reduce chronic disease risk. The DASH approach emphasizes potassiumrich
fruits, vegetables, and low-fat milk products; includes whole grains, nuts,
poultry, and fish; and calls for reduced intakes of sodium, red and processed
meats, sweets, and sugar-containing beverages. In combination with a reduced
sodium intake, DASH is even more effective at lowering blood pressure than either
strategy alone. In addition, DASH lowers the risk of some cancers, heart disease,
and stroke.15 Chapter 18 offers a complete discussion of hypertension and
the dietary recommendations for its prevention and treatment.
Sodium and Bone Loss (Osteoporosis) A high salt intake is also associated with
increased calcium excretion, but its influence on bone loss is less clear. In addition,
potassium may prevent the calcium excretion caused by a high-salt diet.
For these reasons, dietary advice to prevent bone loss parallels that suggested for
hypertension—a DASH eating pattern that is low in sodium and abundant in
potassium-rich fruits and vegetables and calcium-rich low-fat milk.
Sodium in Foods In general, processed foods have the most sodium,
whereas unprocessed foods such as fresh fruits and vegetables have
the least. In fact, as much as 75 percent of the sodium in people's diets
comes from salt added to foods by manufacturers; about 15 percent
comes from salt added during cooking and at the table; and only
10 percent comes from the natural content in foods. Among foods with
the highest sodium density (milligrams of sodium per kcalorie) are those
from fast food and pizza restaurants.16 Because sodium intake tends to
increase as kcalories increase, making food choices based on low sodium
density is a practical and effective way to lower sodium intake.17
To help consumers limit their intake, public health organizations
and policymakers worldwide are calling for manufacturers and restaurants
to reduce sodium in the food supply.18 In addition to reducing
the sodium content of foods, food scientists are designing products to
How To
Cut Salt (and Sodium) Intake
Salt (sodium chloride) is about 40% sodium
and 60% chloride.
● 1 g salt contributes about 400 mg sodium
and 600 mg chloride
● 6 g salt 5 1 tsp
● 1 tsp salt contributes about 2300 mg sodium
and 3700 mg chloride
Most people eat more salt (and therefore sodium)
than they need. Some people can lower
their blood pressure by avoiding highly salted
foods and removing the salt shaker from the
table. Foods eaten without salt may seem less
tasty at first, but with repetition, people can
learn to enjoy the natural flavors of many unsalted
foods. Strategies to cut salt intake include:
● Select fresh or frozen vegetables. If buying
canned vegetables, drain and rinse in water
to remove some of the sodium or select
those labeled low-sodium or no-salt-added.
● Cook with little or no added salt.
● Prepare foods with sodium-free herbs and
spices such as basil, bay leaves, curry,
garlic, ginger, mint, oregano, pepper,
rose mary, and thyme; lemon juice; vinegar;
or wine.
● Add little or no salt at the table; taste
foods before adding salt.
● Read labels with an eye open for sodium. (See
the glossary on p. 61 for terms used to describe
the sodium contents of foods on labels.)
● Select low-salt or salt-free products when
available.
Use these foods sparingly:
● Foods prepared in brine, such as pickles,
olives, and sauerkraut
● Salty or smoked meats, such as bologna,
corned or chipped beef, bacon, frankfurt ers,
ham, lunchmeats, salt pork, sausage, and
smoked tongue
● Salty or smoked fish, such as anchovies,
caviar, salted and dried cod, herring,
sardines, and smoked salmon
● Snack items such as potato chips,
pret zels, salted popcorn, salted nuts,
and crackers
● Condiments such as bouillon cubes; seasoned
salts; MSG; soy, teriyaki, Worcestershire,
and barbeque sauces; prepared
horseradish, ketchup, and mustard
● Cheeses, especially processed types
● Canned and instant soups
● Packaged instant or flavored rice, pasta,
and cereal mixes
❯ TRY IT Compare the sodium contents of 1 ounce of the following foods: a plain bagel, potato chips, and animal crackers
Calcium is the most abundant mineral in the body. It receives much
emphasis in this chapter and in the highlight that follows because an adequate intake
helps grow a healthy skeleton in early life and minimize bone loss in later life.
Calcium Roles in the Body Only 1 percent of the body's calcium is in the body fluids.
The remaining 99 percent of the body's calcium is in the bones (and teeth),
where it plays two roles. First, it is an integral part of bone structure, providing a
rigid frame that holds the body upright and serves as attachment points for muscles,
making motion possible. Second, it serves as a calcium bank, offering a readily
available source of calcium to the body fluids should a drop in blood calcium occur.
As bones begin to form, calcium salts form crystals, called hydroxyapatite, on
a matrix of the protein collagen. During mineralization, as the crystals become
denser, they give strength and rigidity to the maturing bones. As a result, the long
leg bones of children can support their weight by the time they have learned to walk.
Many people have the idea that once a bone is built, it is inert like a rock. Actually,
the bones are gaining and losing minerals continuously in an ongoing process
of remodeling. Growing children gain more bone than they lose, and healthy
adults maintain a reasonable balance. When withdrawals substantially exceed
deposits, problems such as osteoporosis develop (as described in Highlight 12).
The formation of teeth follows a pattern similar to that of bones. The turnover
of minerals in teeth is not as rapid as in bone, however; fluoride hardens and
stabilizes the crystals of teeth, opposing the withdrawal of minerals from them. Although only 1 percent of the body's calcium circulates in the extracellular
and intracellular fluids, its presence there is vital to life. Cells throughout the body
can detect calcium in the extracellular fluids and respond accordingly. Many of
calcium's actions help to maintain normal blood pressure, perhaps by stabilizing
the smooth muscle cells of the blood vessels or by releasing relaxing factors from
the blood vessel cell walls. Extracellular calcium also participates in blood clotting.
The calcium in intracellular fluids binds to proteins within the cells and activates
them. For example, when the protein calmodulin binds with calcium, it activates
the enzymes involved in breaking down glycogen, which releases energy
for muscle contractions. Many such proteins participate in the regulation of muscle
contractions, the transmission of nerve impulses, the secretion of hormones,
and the activation of some enzyme reactions. Calcium in Disease Prevention Calcium may protect against some chronic diseases,
including hypertension.24 Considering the success of DASH in lowering
blood pressure, restricting sodium to treat hypertension may be narrow advice.
The DASH eating pattern is rich in calcium, as well as in magnesium and
potassium—all of which help lower blood pressure.
Calcium-rich foods may play a role in reducing body fat, protecting lean tissue,
and maintaining a healthy body weight.25 Some epidemiological studies suggest
an inverse relationship between calcium
intake and body weight: the higher the
calcium intake, the lower the prevalence
of overweight. Clinical studies, however,
report such small losses (1 to 2 pounds)
as to be statistically insignificant.26 Some
would argue that the real-life benefits
are significant in that weight gains are
diminished and body composition is improved.
27 In addition, calcium-rich foods
suppress the inflammation commonly associated
with overweight, even without
weight loss.28 Importantly, calcium-rich
foods help with weight loss only when
used within an energy-restricted diet.29
Calcium Balance Calcium homeostasis
involves a system of hormones and vitamin
D. Whenever blood calcium falls too
low or rises too high, three organ systems
respond: the intestines, bones, and kidneys.
Figure 12-12 illustrates how vitamin
D and two hormones—parathyroid hormone
and calcitonin—return blood calcium
to normal.
The calcium in bones provides a nearly
inexhaustible bank of calcium for the
blood. The blood borrows and returns
calcium as needed so that even with an
inadequate diet, blood calcium remains
normal—even as bone calcium diminishes
(see Figure 12-13 on p. 390). Blood calcium
changes only in response to abnormal
regulatory control, not to diet. A person
can have an inadequate calcium intake for
years and have no noticeable symptoms.
Only later in life does it become apparent
that bone integrity has been compromised. Blood calcium above normal results in calcium rigor: the muscles contract and
cannot relax. Similarly, blood calcium below normal causes calcium tetany—also
characterized by uncontrolled muscle contraction. These conditions do not reflect a
dietary excess or lack of calcium; they are caused by a lack of vitamin D or by abnormal
secretion of the regulatory hormones. A chronic dietary deficiency of calcium,
or a chronic deficiency due to poor absorption over the years, depletes the bones.
Again: the bones, not the blood, are robbed by a calcium deficiency.
Calcium Absorption Because many factors affect calcium absorption, the most
effective way to ensure adequacy is to increase calcium intake. On average, adults
absorb about 30 percent of the calcium they ingest. The stomach's acidity helps
to keep calcium soluble, and vitamin D helps to make the calcium-binding protein
needed for absorption. This relationship explains why calcium-rich milk is a
good choice for vitamin D fortification.
Whenever calcium is needed, the body increases its calcium absorption. The result
is obvious in the case of a newborn infant, whose calcium absorption is 55 to
60 percent. Similarly, a pregnant woman doubles her absorption of calcium. Growing
children and teens absorb up to 50 percent of the calcium they consume. Then, when
bone growth slows or stops, absorption falls to the adult level of about 30 percent. In
addition, absorption becomes more efficient during times of inadequate intakes.
Many of the conditions that enhance calcium absorption limit its absorption
when they are absent. For example, sufficient vitamin D supports absorption, and
a deficiency impairs it. In addition, fiber in general, and the binders phytate and
oxalate in particular, interfere with calcium absorption, but their effects are relatively
minor in typical US diets. Vegetables with oxalates and whole grains with
phytates are nutritious foods, of course, but they are not useful calcium sources.
Calcium Recommendations Calcium is unlike most other nutrients in that
hormones maintain its blood concentration regardless of dietary intake. As Figure
12-13 shows, when calcium intake is high, the bones benefit; when intake
is low, the bones suffer. Calcium recommendations are therefore based on the
amount needed to retain the most calcium in bones. By retaining the most
calcium possible, the bones can develop to their fullest potential in size and
density—their peak bone mass—within genetic limits.
Calcium recommendations have been set high enough to accommodate a
30 percent absorption rate. Because obtaining enough calcium during growth
helps to ensure that the skeleton will be strong and dense, the recommendation
for adolescents to the age of 18 years is 1300 milligrams daily. Between the ages
of 19 and 50, recommendations are lowered to 1000 milligrams a day; for women
older than 50 and all adults older than 70, recommendations are raised again to
1200 milligrams a day to minimize the bone loss that tends to occur later in life.
Some authorities advocate as much as 1500 milligrams a day for women older than
50. Most people in the United States have calcium intakes below current recommendations.
Those meeting recommendations for calcium are likely to be using calcium
supplements.30 High intakes of calcium from supplements may have adverse
effects such as kidney stone formation. For this reason, a UL has been established.
A high-protein diet increases urinary calcium losses, but does not seem to impair
bone health.31 In fact, protein may even improve calcium absorption and
bone strength. The DRI Committee considered these nutrient interactions in
establishing the RDA for calcium and did not adjust dietary recommendations
based on this information.32
Calcium Food Sources Figure 12-14 shows that calcium is found most abundantly
in a single food group—milk and milk products. The person who doesn't like to
drink milk may prefer to eat cheese or yogurt. Alternatively, milk and milk products
can be concealed in foods. Powdered fat-free milk can be added to casseroles,
soups, and other mixed dishes during preparation; 5 heaping tablespoons offer the
equivalent of 1 cup of milk. This simple step is an excellent way for older women
to obtain not only extra calcium, but more protein, vitamins, and minerals as well.
It is especially difficult for children who don't drink milk to meet their calcium
needs. The consequences of drinking too little milk during childhood and
adolescence persist into adulthood. Women who seldom drank milk as children
have lower bone density and greater risk of fractures than those who drank milk
regularly. It is possible for people who do not drink milk to obtain adequate calcium,
but only if they carefully select other calcium-rich foods.
> DIETARY GUIDELINES FOR AMERICANS
Choose foods that provide more calcium, a nutrient of concern in American
diets. The best sources of calcium are milk and milk products.
Many people, for a variety of reasons, cannot or do not drink milk. Some cultures
do not use milk in their cuisines; some vegetarians exclude milk as well as
meat; and some people are allergic to milk protein or are lactose intolerant. Others
simply do not enjoy the taste of milk. These people need to find other foods to help
meet their calcium needs. Some brands of tofu, corn tortillas, some nuts (such as
almonds), and some seeds (such as sesame seeds) can supply calcium for the person
who doesn't use milk products. A slice of most breads contains only about 5
to 10 percent of the calcium found in milk, but it can be a major source for people
who eat many slices because the calcium is well absorbed. Oysters are also a rich
source of calcium, as are small fish eaten with their bones, such as canned sardines.
Among the vegetables, mustard and turnip greens, bok choy, kale, parsley,
watercress, and broccoli are good sources of available calcium. So are some seaweeds
such as the nori popular in Japanese cooking. Some dark green, leafy vegetables—notably spinach and Swiss chard—appear to be calcium-rich but actually
provide little, if any, calcium because they contain binders that limit absorption.
It would take 8 cups of spinach—containing six times as much calcium
as 1 cup of milk—to deliver the equivalent in absorbable calcium.
With the exception of foods such as spinach that contain calcium binders, the
calcium content of foods is usually more important than bioavailability. Consequently,
recognizing that people eat a variety of foods containing calcium, the DRI
Committee did not adjust for calcium bioavailability when setting recommendations.
Figure 12-15 ranks selected foods according to their calcium bioavailability.
Some mineral waters provide as much as 500 milligrams of calcium per liter,
offering a convenient way to meet both calcium and water needs. Similarly, calciumfortified
orange juice and other fruit and vegetable juices allow a person to obtain
both calcium and vitamins easily. Other examples of calcium-fortified foods include
high-calcium milk (milk with extra calcium added) and calcium-fortified cereals.
Fortified juices and foods help consumers increase calcium intakes, but depending
on the calcium sources, the bioavailability may be significantly less than quantities
listed on food labels. The accompanying "How To" feature describes a quick way to
estimate calcium intake. Highlight 12 discusses calcium supplements.
FIGURE 12-13 Maintaining Blood
Calcium from the Diet and from the Bones
With an adequate
intake of calcium-rich
food, blood calcium
remains normal . . .
With a dietary
deficiency, blood
calcium still remains
normal . . .
. . . and bones deposit
calcium. The result is
strong, dense bones.
. . . because bones
give up calcium to
the blood. The result
is weak, osteoporotic
bones. Estimate Your Calcium
Intake
Most dietitians have devel oped useful
shortcuts to help them estimate nutrient
intakes and "see" inadequacies in the diet.
They can tell at a glance whether a day's
meals fall short of calcium recommendations,
for example.
To estimate calcium intakes, keep two
bits of information in mind:
● A cup of milk provides about 300 milligrams
of calcium.
● Adults need between 1000 and 1200
milligrams of calcium per day, which
represents 3 to 4 cups of milk—or the
equivalent:
1000 mg 4 300 mg/c = 31∕3 c
1200 mg 4 300 mg/c = 4 c
If a person drinks 3 to 4 cups of milk a day,
it's easy to see that calcium needs are
being met. If not, it takes some de tective
work to identify the other sources and
estimate total calcium intake.
To estimate a person's daily calcium
intake, use this shortcut, which compares
the calcium in calcium-rich foods
to the calcium content of milk. The calcium
in a cup of milk is assigned 1 point,
and the goal is to attain 3 to 4 points per
day. Foods are given points as follows:
● 1 c milk, yogurt, or fortified soy milk
or 1½ oz cheese = 1 point
● 4 oz canned fish with bones (sardines)
= 1 point
● 1 c ice cream, cottage cheese, or
calcium-rich vegetable (see the text)
= ½ point
Then, because other foods also contrib ute
small amounts of calcium, together they
are given a point.
● Well-balanced diet containing a vari ety of
foods 5 1 point
Now consider a day's meals with calcium
in mind. Cereal with 1 cup of milk for breakfast
(1 point for milk), a ham and cheese sub
sandwich for lunch (1 point for cheese), and
a cup of broccoli and lasagna for dinner
(½ point for calcium-rich vegetable and
1 point for cheese in lasagna)—plus 1 point
for all other foods eaten that day—adds
up to 4½ points. This shortcut estimate
indicates that cal cium recommendations
have been met, and a diet analysis of these
few foods reveals a calcium intake of more
than 1000 milligrams. By knowing the best
sources of each nutrient, you can learn to
scan the day's meals and quickly see if you
are meeting your daily goals.
HIGHLIGHT 12
Osteoporosis and Calcium
❯ LEARN IT Describe factors that contribute to the development
of osteoporosis and strategies to prevent it.
Osteoporosis becomes apparent during the later years, but it develops
much earlier—and without warning. Few people are aware
that their bones are being robbed of their strength. The problem often
first becomes evident when someone's hip suddenly gives way.
People say, "She fell and broke her hip," but in fact the hip may have
been so fragile that it broke before she fell. Even bumping into a table
may be enough to shatter a porous bone into fragments so numerous
and scattered that they cannot be reassembled. Removing them and
replacing them with an artificial joint requires major surgery. An estimated
258,000 people in the United States are hospitalized each year
because of hip fractures related to osteoporosis. About one in five die
of complications within a year; one in three will never walk or live
independently again.1 Their quality of life slips downward.
This highlight examines low bone density and osteoporosis, one
of the most prevalent diseases of aging, affecting an estimated
52 million people in the United States—most of them women older
than 50.2 It reviews the many factors that contribute to the 2 million
fractures in the bones of the hips, vertebrae, wrists, arms, and ankles
each year. And it presents strategies to reduce the risks, paying special
attention to the role of dietary calcium.
Bone Development
and Disintegration
Bone has two compartments: the outer, hard shell of cortical bone and
the inner, lacy matrix of trabecular bone. (The glossary defines these
and other bone-related terms.) Both can lose minerals, but in different
ways and at different rates. The first photograph in Figure H12-1 shows a
human leg bone sliced lengthwise, exposing the lacy, calcium-containing
crystals of trabecular bone. These crystals give up calcium to the blood
when the diet runs short, and they take up calcium again when the supply
is plentiful (review Figure 12-13 on p. 390). For people who have eaten
calcium-rich foods throughout the bone-forming years of their youth,
these deposits make bones dense and provide a rich reservoir of calcium. Surrounding and protecting the trabecular bone is a dense, ivorylike exterior
shell—the cortical bone. Cortical bone composes the shafts of the
long bones, and a thin cortical shell caps the ends of the bones too. Both
compartments confer strength on bone: cortical bone provides the sturdy
outer wall, and trabecular bone provides support along the lines of stress.
The two types of bone handle calcium in different ways. Supplied
with blood vessels and metabolically active, trabecular bone is
sensitive to hormones that govern day-to-day deposits and withdrawals
of calcium. It readily gives up minerals whenever blood calcium
needs replenishing. Losses of trabecular bone start becoming significant
for men and women in their 30s, although losses can occur whenever
calcium withdrawals exceed deposits. Cortical bone also gives
up calcium, but slowly and at a steady pace. Cortical bone losses typically
begin at about age 40 and continue slowly but surely thereafter.
As bone loss continues, bone density declines, and osteoporosis
becomes apparent (see Figure H12-1). Bones become so fragile that
even the body's own weight can overburden the spine—vertebrae may
suddenly disintegrate and crush down, painfully pinching major nerves.
Or the vertebrae may compress into wedge shapes, forming what is often called a "dowager's hump," the posture many older people assume
as they "grow shorter." Figure H12-2 (p. 402) shows the effect
of compressed spinal bone on a woman's height and posture. Because
both the cortical shell and the trabecular interior weaken, breaks most
often occur in the hip, as mentioned in the introductory paragraph.
Physicians can determine bone loss and diagnose osteoporosis
by measuring bone density using dual-energy X-ray absorptiometry
(DEXA scan).3 They also consider risk factors for osteoporosis,
including age, personal and family history of fractures, and physical
inactivity. Table H12-1 summarizes the major risk factors for osteoporosis. The more risk factors that apply to a person, the greater
the chances of bone loss. Notice that several risk factors that are influential
in the development of osteoporosis—such as age, gender,
and genetics—cannot be changed. Other risk factors—such as diet,
physical activity, body weight, smoking, and alcohol use—are personal
behaviors that can be changed. By eating a calcium-rich, wellbalanced
diet; being physically active; abstaining from smoking; and
drinking alcohol in moderation (if at all), people can defend themselves
against osteoporosis. These decisions are particularly important for
those with other risk factors that cannot be changed.
Whether a person develops osteoporosis seems to depend on
the interactions of several factors, including nutrition. The strongest
predictor of bone density is age. Age and Bone Calcium
Two major stages of life are critical in the development of osteoporosis.
The first is the bone-acquiring stage of childhood and adolescence. The
second is the bone-losing decades of late adulthood, especially in women
after menopause. The bones gain strength and density all through the
growing years and into young adulthood. As people age, the cells that build
bone gradually become less active, but those that dismantle bone continue
working. The result is that bone loss exceeds bone formation. Some bone
loss is inevitable, but losses can be curtailed by maximizing bone mass.
Maximizing Bone Mass
To maximize bone mass, the diet must deliver an adequate supply of
calcium during the first three decades of life. Children and teens who consume milk products and get enough calcium have denser bones
than those with inadequate intakes. With little or no calcium from the
diet, the body must depend on bone to supply calcium to the blood—
bone mass diminishes, and bones lose their density and strength.
When people reach the bone-losing years of middle age, those who
formed dense bones during their youth have the advantage. They simply
have more bone starting out and can lose more before suffering ill
effects. Figure H12-3 demonstrates this effect.
Minimizing Bone Loss
Not only does dietary calcium build strong bones in youth, but it remains
important in protecting against losses in the later years. Unfortunately,
calcium intakes of older adults are typically low, and calcium absorption
declines after menopause. The kidneys do not activate vitamin D as well as
they did earlier (recall that vitamin D enhances calcium absorption). Also,
sunlight is needed to form vitamin D, and many older people spend little or
no time outdoors in the sunshine. For these reasons, and because intakes
of vitamin D are typically low anyway, blood levels of vitamin D decline.
Some of the hormones that regulate bone and calcium metabolism—
parathyroid hormone, calcitonin, and estrogen—also change with age
and accelerate bone loss. Together, these age-related factors contribute
to bone loss: inefficient bone remodeling, reduced calcium intakes,
impaired calcium absorption, poor vitamin D status, and hormonal
changes that favor bone mineral withdrawal.
Gender and Hormones
After age, gender is the next strongest predictor of osteoporosis. The
sex hormones play a major role in regulating the rate of bone turnover.4
Men have greater bone density than women at maturity, and women have greater losses than men in later life. Consequently, men develop
bone problems about 10 years later than women, and women account
for two out of three cases of osteoporosis.
Menopause imperils women's bones. Bone dwindles rapidly
when the hormone estrogen diminishes and menstruation ceases.
The lack of estrogen contributes to the release of cytokines that produce
inflammation and accelerate bone loss.5 Women may lose up to
20 percent of their bone mass during the 6 to 8 years following menopause.
Eventually, losses taper off so that women again lose bone
at the same rate as men their age. Losses of bone minerals continue
throughout the remainder of a woman's lifetime, but not at the freefall
pace of the menopause years (review Figure H12-3).
Rapid bone losses also occur when young women's ovaries fail to produce
enough estrogen, causing menstruation to cease. In some cases, diseased
ovaries are to blame and must be removed; in others, the ovaries fail to
produce sufficient estrogen because the women suffer from anorexia nervosa
and have unreasonably restricted their body weight (see Highlight 8).
The amenorrhea and low body weights explain much of the bone loss seen
in these young women, even years after diagnosis and treatment.
Estrogen therapy may help some women prevent further bone
loss and reduce the incidence of fractures. Because estrogen therapy
may increase the risks for breast cancer, women must carefully
weigh any potential benefits against the possible dangers. A
combination of drugs or of hormone replacement and a drug may
be most beneficial.
Several drug therapies have been developed to inhibit bone loss
and enhance bone formation.6 The FDA has approved the following
drugs to prevent or treat osteoporosis: biophosphates, calcitonin, estrogens,
estrogen antagonists, and parathyroid hormone.7
Some women who choose not to use estrogen therapy turn to soy
as an alternative treatment. Interestingly, the phytochemicals commonly
found in soy mimic the actions of estrogen in the body. Research
results have been mixed and controversial, but overall seem
to indicate a lack of benefit for soy and its phytochemicals in helping
to prevent the rapid bone losses of the menopause years.8 As is true
of all herbal products, there may be risks associated with their use,
and in the case of soy, evidence is lacking that the benefits clearly
outweigh the potential risks.9 Because the risks and benefits vary depending
on each person's medical history, women should discuss soy
options with their physicians.
As in women, sex hormones appear to play a key role in men's
bone loss as well.10 Other common causes of osteoporosis in men include
corticosteroid use and alcohol abuse.
Genetics
Risks of osteoporosis appear to run along racial lines and reflect genetic
differences in bone development. African Americans, for example,
seem to use and retain calcium more efficiently than Caucasians.
Consequently, even though their calcium intakes are typically lower,
black people have denser bones than white people do. Greater bone
density expresses itself in less bone loss, fewer fractures, and a lower
rate of osteoporosis among blacks. The exact role of genetics is unclear.11 Most likely, genes influence
both the peak bone mass achieved during growth and the bone loss
incurred during the later years. The extent to which a given genetic potential
is realized, however, depends on many outside factors. Diet and
physical activity, for example, can maximize peak bone density during
growth, whereas alcohol and tobacco abuse can accelerate bone losses
later in life. Importantly, these factors are within a person's control.
Physical Activity and Body Weight
Physical activity may be the single most important factor supporting
bone growth during adolescence.12 Muscle strength and bone strength
go together. When muscles work, they pull on the bones, stimulating
them to grow denser. The hormones that promote new muscle growth
also favor the building of
bone. As a result, active
bones are denser and stronger
than sedentary bones.
Both the muscle contraction
and the gravitational
pull of the body's
weight create a load that
benefits bone metabolism.
To keep bones healthy, a
person should engage in
weight training or weightbearing
endurance activities
(such as tennis and
jogging or sprint cycling)
regularly.13 Regular physical
activity combined with
an adequate calcium intake
helps to maximize bone
density in adolescence.
Adults can also maximize
and maintain bone density with a regular program of weight training. Even
past menopause, when most women are losing bone, weight training improves
bone density.
Heavier body weights and weight gains place a similar stress on
the bones and promote their density. In contrast, weight losses reduce
bone density and increase the risk of fractures—in part because
energy restriction diminishes calcium absorption and compromises
calcium balance. As mentioned in Highlight 8, the relative energy deficiency
that results from a combination of restricted energy intake and
extreme daily exercise reliably predicts bone loss.
Smoking and Alcohol
Add bone damage to the list of ill consequences associated with smoking.
The bones of smokers are less dense than those of nonsmokers—
even after controlling for differences in age, body weight, and physical
activity habits. Fortunately, the damaging effects can be reversed
with smoking cessation. Blood indicators of beneficial bone activity are apparent 6 weeks after a person stops smoking. In time, bone density
is similar for former smokers and nonsmokers.
People who abuse alcohol often suffer from osteoporosis and experience
more bone breaks than others. Several factors appear to be
involved. Alcohol enhances fluid excretion, leading to excessive calcium
losses in the urine; upsets the hormonal balance required for
healthy bones; slows bone formation, leading to lower bone density;
stimulates bone breakdown; and increases the risk of falling.
Dietary Calcium
Diets that are habitually low in calcium increase the risk of fractures
and osteoporosis.14 For older adults, an adequate calcium intake alone
cannot protect against bone fractures. Bone strength later in life depends
primarily on how well the bones were built during childhood and
adolescence. Adequate calcium nutrition during the growing years is
essential to achieving optimal peak bone mass. Simply put, growing
children who do not get enough calcium do not develop strong bones.
For this reason, the DRI Committee recommends 1300 milligrams of
calcium per day for everyone 9 through 18 years of age. Unfortunately,
few girls meet the r ecommendations for calcium during these boneforming
years. (Boys generally obtain intakes close to those recommended
because they eat more food.) Consequently, most girls start
their adult years with less-than-optimal bone density. As adults,
women rarely meet their recommended intakes of 1000 to 1200 milligrams
from food. Some authorities suggest 1500 milligrams of calcium
for postmenopausal women who are not receiving estrogen.
Other Nutrients
Much research has focused on calcium, but other nutrients support bone
health too. Adequate protein protects bones and reduces the likelihood
of hip fractures. As mentioned earlier, vitamin D is needed to maintain
calcium metabolism and optimal bone health. Vitamin K decreases bone
turnover and protects against hip fractures. Vitamin C may slow bone
losses. The minerals magnesium and potassium also help to maintain
bone mineral density. Vitamin A is needed in the bone-remodeling process,
but too much vitamin A may be associated with osteoporosis. Carotenoids
may inhibit bone loss. Omega-3 fatty acids may help preserve
bone integrity. Additional research points to the bone benefits not of
a specific nutrient, but of a diet rich in fruits, vegetables, and whole
grains.15 In contrast, diets containing too much salt are associated with
bone losses. Similarly, diets containing too many colas or commercially
baked snack and fried foods are associated with low bone mineral density.
Clearly, a well-balanced diet that depends on all the food groups to
supply a full array of nutrients is central to bone health.
A Perspective on Calcium
Supplements
Bone health depends, in part, on calcium. People who do not consume
milk products or other calcium-rich foods in amounts that provide
even half the recommendation should consider consulting a registered dietitian nutritionist who can assess the diet and suggest food choices
to correct any inadequacies. Calcium from foods may support bone
health better than calcium from supplements. For those who are unable
to consume enough calcium-rich foods, however, taking calcium
supplements—especially in combination with vitamin D—may help
to enhance bone density and protect against bone loss and fractures.16
Because some research suggests that calcium supplements may increase
the risk of heart attacks and strokes, women should consult
their physicians when making this decision.17
An estimated 60 percent of women aged 60 and over take calcium
supplements.18 Selecting a calcium supplement requires a little
investigative work to sort through the many options. Before examining
calcium supplements, recognize that multivitamin-mineral pills contain
little or no calcium. The label may list a few milligrams of calcium, but
remember that the recommended intake is a gram (1000 milligrams) or
more for adults.
Calcium supplements are typically sold as compounds of calcium
carbonate (common in antacids and fortified chocolate candies),
citrate, gluconate, lactate, malate, or phosphate. These supplements
often include magnesium, vitamin D, or both. In addition, some calcium
supplements are made from bone meal, oyster shell, or dolomite
(limestone). Many calcium supplements, especially those derived
from these natural products, contain lead—which impairs health in
numerous ways, as Chapter 13 points out. Fortunately, calcium interferes
with the absorption and action of lead in the body.
The first question to ask is how much calcium the supplement provides.
Most calcium supplements provide between 250 and 1000 milligrams
of calcium. To be safe, total calcium intake from both foods
and supplements should not exceed the UL. Read the label to find out
how much a dose supplies. Unless the label states otherwise, supplements
of calcium carbonate are 40 percent calcium; those of calcium
citrate are 21 percent; lactate, 13 percent; and gluconate, 9 percent.
Select a low-dose supplement and take it several times a day rather
than taking a large-dose supplement all at once. Taking supplements
in doses of 500 milligrams or less improves absorption. Small doses
also help ease the GI distress (constipation, intestinal bloating, and
excessive gas) that sometimes accompanies calcium supplement use.
The next question to ask is how well the body absorbs and uses
the calcium from various supplements. Most healthy people absorb
calcium equally well from milk and any of these supplements: calcium
carbonate, citrate, or phosphate. More important than supplement
solubility is tablet disintegration. When manufacturers compress large
quantities of calcium into small pills, the stomach acid has difficulty
penetrating the pill. To test a supplement's ability to dissolve, drop
it into a 6-ounce cup of vinegar, and stir occasionally. A high-quality
formulation will dissolve within a half-hour.
Finally, people who choose supplements must take them regularly.
Furthermore, consideration should be given to the best time to take
the supplements. To circumvent adverse nutrient interactions, take
calcium supplements between, not with, meals. (Importantly, do not
take calcium supplements with iron supplements or iron-rich meals;
calcium inhibits iron absorption.) To enhance calcium absorption, take
supplements with meals. If such contradictory advice drives you crazy, reconsider the benefits of food sources of calcium. Most experts
agree that foods are the best source of most nutrients.
Some Closing Thoughts
Unfortunately, many of the strongest risk factors for osteoporosis
are beyond people's control: age, gender, and genetics. But several
strategies are effective for prevention. First, ensure an optimal peak
bone mass during childhood and adolescence by eating a balanced diet rich in calcium and vitamin D and by engaging in regular physical
activity. Then, maintain that bone mass in early adulthood by
continuing those healthy diet and activity habits, abstaining from
cigarette smoking and using alcohol moderately, if at all. Finally,
minimize bone loss in later life by maintaining an adequate nutrition
and exercise regimen, and, especially for older women, consult
a physician about bone density tests, calcium supplements, or other
drug therapies that may be effective both in preventing bone loss
and in restoring lost bone.19 The reward is the best possible chance
of preserving bone health throughout life.
Iron is an essential nutrient, vital to many of the cells' activities, but it
poses a problem for millions of people. Some people simply don't eat enough
iron- containing foods to support their health optimally, whereas others absorb
so much iron that it threatens their health. Iron exemplifies the principle that
both too little and too much of a nutrient in the body can be harmful. In its
wisdom, the body has several ways to maintain iron balance, protecting against
both deficiency and toxicity.
Iron Roles in the Body Iron has the knack of switching back and forth between
two ionic states. In the reduced state, iron has lost two electrons and therefore has
a net positive charge of two; it is known as ferrous iron (Fe++). In the oxidized state,
iron has lost a third electron, has a net positive charge of three, and is known as
ferric iron (Fe+++). Ferrous iron can be oxidized to ferric iron, and ferric iron can
be reduced to ferrous iron. By doing so, iron can serve as a cofactor to enzymes
involved in the numerous oxidation-reduction reactions that commonly occur
in all cells. Enzymes involved in making amino acids, collagen, hormones, and
neurotransmitters all require iron. (For details about ions, oxidation, and reduction,
see Appendix B.)
Iron forms a part of the electron carriers that participate in the electron transport
chain (discussed in Chapter 7).* These carriers transfer hydrogens and electrons to
oxygen, forming water, and in the process, make ATP for the cells' energy use.
Most of the body's iron is found in two proteins: hemoglobin in the red blood
cells and myoglobin in the muscle cells. In both, iron helps accept, carry, and
then release oxygen.
Iron Absorption The body conserves iron. Because it is difficult to excrete iron
once it is in the body, balance is maintained primarily through absorption. More
iron is absorbed when stores are empty and less is absorbed when stores are full.
Special proteins help the body absorb iron from food (see Figure 13-3).2 The
iron-storage protein ferritin captures iron from food and stores it in the cells
of the small intestine. When the body needs iron, ferritin releases some iron to
an iron transport protein called transferrin. If the body does not need iron, it is
carried out when the intestinal cells are shed and excreted in the feces; intestinal
cells are replaced about every 3 to 5 days. By holding iron temporarily, these cells
control iron absorption by either delivering iron when the day's intake falls short
or disposing of it when intakes exceed needs.
Iron absorption depends in part on its dietary source. Iron occurs in two forms
in foods: as heme iron, which is found only in foods derived from the flesh of animals,
such as meats, poultry, and fish and as nonheme iron, which is found in both
plant-derived and animal-derived foods (see Figure 13-4). On average, heme iron
represents about 10 percent of the iron a person consumes in a day. Even though
heme iron accounts for only a small proportion of the intake, it is so well absorbed
that it contributes significant iron. About 25 percent of heme iron and 17 percent of
nonheme iron is absorbed, depending on dietary factors and the body's iron stores.3
In iron deficiency, absorption increases. In iron overload, absorption declines.
Heme iron has a high bioavailability and is not inf luenced by dietary factors.
In contrast, several dietary factors influence nonheme iron absorption (see
Table 13-1).4 Meat, fish, and poultry contain not only the well-absorbed heme
iron, but also a peptide (sometimes called the MFP factor) that promotes the absorption of nonheme iron from other foods eaten at the same meal. Vitamin
C (ascorbic acid) also enhances nonheme iron absorption from foods eaten at
the same meal by capturing the iron and keeping it in the reduced ferrous form,
ready for absorption. Some acids (such as citric acid) and sugars (such as fructose)
also enhance nonheme iron absorption.
Some dietary factors bind with nonheme iron, inhibiting absorption. These
factors include the phytates in legumes, whole grains, and rice; the vegetable proteins
in soybeans, other legumes, and nuts; the calcium in milk; and the polyphenols
(such as tannic acid) in tea, coffee, grain products, oregano, and red wine.
The many dietary enhancers, inhibitors, and their combined effects make it
difficult to estimate iron absorption. Most of these factors exert a strong influence
individually, but not when combined with the others in a meal. Furthermore, the
impact of the combined effects diminishes when a diet is evaluated over several
days. When multiple meals are analyzed together, three factors appear to be most
relevant: MFP factor and vitamin C as enhancers and phytates as inhibitors. Overall, about 18 percent of dietary iron is absorbed from mixed diets and
only about 10 percent from vegetarian diets. As you might expect, vegetarian
diets do not have the benefit of easy-to-absorb heme iron or the help of the MFP
factor in enhancing absorption. In addition to dietary influences, iron absorption
also depends on an individual's health, stage in the life cycle, and iron status.
Absorption can be as low as 2 percent in a person with GI disease or as high as
35 percent in a rapidly growing, healthy child. The body adapts to absorb more
iron when a person's iron stores fall short or when the need increases for any reason
(such as pregnancy). The body makes more ferritin to absorb more iron from
the small intestine and more transferrin to carry more iron around the body.
Similarly, when iron stores are sufficient, the body adapts to absorb less iron.
Iron Transport and Storage The blood transport protein transferrin delivers iron
to the bone marrow and other tissues. The bone marrow uses large quantities of
iron to make new red blood cells, whereas other tissues use less. Surplus iron is
stored in the protein ferritin, primarily in the liver, but also in the bone marrow
and spleen. When dietary iron has been plentiful, ferritin is constantly and rapidly
made and broken down, providing an ever-ready supply of iron. When iron
concentrations become abnormally high, the liver converts some ferritin into another
storage protein called hemosiderin. Hemosiderin releases iron more slowly
than ferritin does. Storing excess iron in hemosiderin protects the body against
the damage that free iron can cause. Free iron acts as a free radical, attacking cell
lipids, DNA, and protein. (See Highlight 11 for more information on free radicals
and the damage they can cause.)
The average red blood cell lives about 4 months; then the spleen and liver cells
remove it from the blood, take it apart, and prepare the degradation products
for excretion or recycling. The iron is salvaged: the liver attaches it to transferrin,
which transports it back to the bone marrow to be reused in making new
red blood cells. Thus, although red blood cells live for only about 4 months, the
iron recycles through each new generation of cells (see Figure 13-5). The body
loses some iron daily via the GI tract and, if bleeding occurs, in blood. Only tiny amounts of iron are lost in urine, sweat, and shed skin. Iron excretion differs
for men and women. On average, men and women lose about 1.0 milligram
of iron per day, with women losing additional iron in menses; menstrual losses
vary considerably, but over a month, they average about 0.5 milligram per day.
Maintaining iron balance depends on the careful regulation of iron absorption,
transport, storage, recycling, and losses. Central to the regulation of iron
balance is the hormone hepcidin.5 Produced by the liver, hepcidin helps to
maintain blood iron within the normal range by limiting absorption from the
small intestine and controlling release from the liver, spleen, and bone marrow.
Hepcidin production increases in iron overload and decreases in iron deficiency.
Iron Deficiency Worldwide, iron deficiency is the most common nutrient deficiency,
with iron-deficiency anemia affecting 1.5 to 2.0 billion people—
mostly preschool children and pregnant women.7 In the United States, iron
deficiency is less prevalent, but it still affects about 10 percent of toddlers, adolescent
girls, and women of childbearing age. Iron deficiency is also relatively common
among those who are overweight. The association between iron deficiency
and obesity has yet to be explained, but researchers are currently examining the
relationships between the inflammation that develops with excess body fat and
reduced iron absorption.8 The increased production of hepcidin in obesity may
also help to explain the relationship between obesity and iron deficiency.9 Preventing
and correcting iron deficiency are high priorities.
Some stages of life demand more iron but provide less, making deficiency
likely.10 Women in their reproductive years are especially prone to iron deficiency
because of repeated blood losses during menstruation. Pregnancy demands
additional iron to support the added blood volume, growth of the fetus, and
blood loss during childbirth. Infants and young children receive little iron from
their high-milk diets, yet need extra iron to support their rapid growth and brain
development.* Iron deficiency among toddlers in the United States is common.
The rapid growth of adolescence, especially for males, and the menstrual losses
of females also demand extra iron that a typical teen diet may not provide. An
adequate iron intake is especially important during these stages of life.
Bleeding from any site incurs iron losses.** In some cases, such as an active
ulcer, the bleeding may not be obvious, but even small chronic blood losses significantly
deplete iron reserves. In developing countries, blood loss is often brought
on by malaria and parasitic infections of the GI tract. People who donate blood
regularly also incur losses and may benefit from iron supplements. As mentioned,
menstrual losses can be considerable as they tap women's iron stores regularly.
Assessment of Iron Deficiency Iron deficiency develops in stages. This section
provides a brief overview of how to detect these stages, and Appendix E provides
more details. In the first stage of iron deficiency, iron stores diminish. Measures of
serum ferritin (in the blood) reflect iron stores and are most valuable in assessing
iron status at this earliest stage. Unfortunately, serum ferritin increases with infections,
which interferes with an accurate diagnosis and estimates of prevalence.11
The second stage of iron deficiency is characterized by a decrease in transport
iron: serum iron falls, and the iron-carrying protein transferrin increases
(an adaptation that enhances iron absorption). Together, measurements of serum
iron and transferrin can determine the severity of the deficiency—the more
transferrin and the less iron in the blood, the more advanced the deficiency is.
Transferrin saturation—the percentage of transferrin that is saturated with iron—
decreases as iron stores decline.
The third stage of iron deficiency occurs when the lack of iron limits hemoglobin
production. Now the hemoglobin precursor, erythrocyte protoporphyrin,
begins to accumulate as hemoglobin and hematocrit values decline. Hemoglobin and hematocrit tests are easy, quick, and inexpensive, so they are
the tests most commonly used in evaluating iron status. Their usefulness in detecting
iron deficiency is limited, however, because they are late indicators. Furthermore,
other nutrient deficiencies and medical conditions can influence their
values.
Iron Deficiency and Anemia Notice that iron deficiency and iron-deficiency anemia
are not the same: people may be iron deficient without being anemic. The
term iron deficiency refers to depleted body iron stores without regard to the degree
of depletion or to the presence of anemia. The term iron-deficiency anemia
refers to the severe depletion of iron stores that results in a low hemoglobin concentration.
In iron-deficiency anemia, hemoglobin synthesis decreases, resulting
in red blood cells that are pale (hypochromic) and small (microcytic), as shown
in Figure 13-6. Without adequate iron, these cells can't carry enough oxygen
from the lungs to the tissues. Energy metabolism in the cells falters. The result
is fatigue, weakness, headaches, apathy, pallor, and poor resistance to cold temperatures.
Because hemoglobin is the bright red pigment of the blood, the skin
of a fair person who is anemic may become noticeably pale. In a dark-skinned
person, the tongue and eye lining, normally pink, is very pale.
The fatigue that accompanies iron-deficiency anemia differs from the tiredness
a person experiences from a simple lack of sleep. People with anemia feel
fatigue only when they exert themselves. Consequently, their work productivity,
voluntary activities, and athletic performance decline.12 Iron supplementation
can relieve the fatigue and improve the body's response to physical activity.13
(The iron needs of physically active people and the special iron deficiency known
as sports anemia are discussed in Chapter 14.) Iron Deficiency and Behavior Long before the red blood cells are affected and
anemia is diagnosed, a developing iron deficiency affects behavior.14 Even at
slightly lowered iron levels, energy metabolism is impaired and neurotransmitter
synthesis is altered, reducing physical work capacity and mental productivity.
15 Without the physical energy and mental alertness to work, plan, think, play,
sing, or learn, people simply do less. They have no obvious deficiency symptoms;
they just appear unmotivated and apathetic.
Many of the symptoms associated with iron deficiency are easily mistaken for
behavioral or motivational problems. A restless child who fails to pay attention
in class might be thought contrary. An apathetic homemaker who has let housework
pile up might be thought lazy. No responsible dietitian would ever claim
that all behavioral problems are caused by nutrient deficiencies, but poor nutrition
is always a possible contributor to problems like these. When investigating
a behavioral problem, check the adequacy of the diet and seek a routine physical
examination before undertaking more expensive, and possibly more harmful,
treatment options. If iron deficiency is the problem, then treatment with iron supplements
may improve mood, cognitive skills, and physical performance. The effects
of iron deficiency on children's behavior are discussed further in Chapter 16.
Iron Deficiency and Pica A curious behavior seen in some iron-deficient people,
especially in women and children of low-income groups, is pica—the craving
and consumption of ice, chalk, starch, and other nonfood substances. These substances
contain no iron and cannot remedy a deficiency; in fact, clay actually
inhibits iron absorption, which may explain the iron deficiency that accompanies
such behavior. Pica is poorly understood. Its cause is unknown, but researchers
hypothesize that it may be motivated by hunger, nutrient deficiencies, or an attempt
to protect against toxins or microbes.16 The consequence of pica is anemia.
Iron Overload As mentioned earlier, because too much iron can be toxic, its levels
in the body are closely regulated and absorption normally decreases when
iron stores are full.17 Even a diet that includes fortified foods usually poses no
risk for most people, but some individuals are vulnerable to excess iron. Once
considered rare, iron overload has emerged as an important disorder of iron metabolism
and regulation.
The iron overload disorder known as hemochromatosis is caused by a genetic
failure to prevent unneeded iron in the diet from being absorbed.18 Research suggests
that just as insulin supports normal glucose homeostasis and its absence
or ineffectiveness causes diabetes, the hormone hepcidin supports iron homeostasis
and its deficiency or (rarely) resistance causes hemochromatosis.19 Other
causes of iron overload include repeated blood transfusions (which bypass the
intestinal defense), massive doses of supplementary iron (which overwhelm the
intestinal defense), and other rare metabolic disorders.
Some of the signs and symptoms of iron overload are similar to those of iron
deficiency: apathy, lethargy, and fatigue. Therefore, taking iron supplements before
assessing iron status is clearly unwise; hemoglobin tests alone would fail to
make the distinction because excess iron accumulates in storage. Iron overload
assessment tests measure transferrin saturation and serum ferritin.
Iron overload is characterized by a toxic accumulation of iron in the liver, heart,
joints, and other tissues. Excess iron in these tissues causes free-radical damage.20
Infections are likely because viruses and bacteria thrive on iron-rich blood. Symptoms
are most severe in alcohol abusers because alcohol damages the small intestine,
further impairing its defenses against absorbing excess iron. Untreated iron overload
increases the risks of diabetes, liver cancer, heart disease, and arthritis.21 Currently,
treatment involves phlebotomy, which removes blood from the body, and chelation
therapy, which uses a chelate to form a complex with iron and promote its excretion.
22 Research targeting the activity of hepcidin is active and promising.23
Iron overload is much more common in men than in women and is twice as
prevalent among men as iron deficiency. The widespread fortification of foods
with iron makes it difficult for people with hemochromatosis to follow a low-iron diet, and greater dangers lie in the indiscriminate use of iron and vitamin C
supplements. Vitamin C not only enhances iron absorption, but also releases
iron from ferritin, allowing free iron to wreak the damage typical of free radicals.
Thus vitamin C acts as a prooxidant when taken in high doses. (See Highlight 11
for a discussion of free radicals and their effects on disease development.)
Zinc Zinc is an essential trace element required for numerous metabolic reactions.
26 Virtually all cells contain zinc, but the highest concentrations are found
in muscle and bone.
Zinc Roles in the Body Zinc supports the work of hundreds of proteins in the
body, such as the metalloenzymes, which participate in a variety of metabolic
processes, and transcription factors, which regulate gene expression.* In addition,
zinc stabilizes cell membranes and DNA, helping to strengthen antioxidant
defenses against free-radical attacks. Zinc also assists in immune function and in
growth and development. Zinc participates in the synthesis, storage, and release
of the hormone insulin in the pancreas, although it does not appear to play a direct
role in insulin's action. Zinc interacts with platelets in blood clotting, affects
thyroid hormone function, and influences behavior and learning performance.
It is needed to produce the active form of vitamin A (retinal) in visual pigments
and the retinol-binding protein that transports vitamin A. It is essential to normal
taste perception, wound healing, sperm production, and fetal development.
A zinc deficiency impairs all these and other functions, underlining the vast importance
of zinc in supporting the body's proteins.
Zinc Absorption The body's handling of zinc resembles that of iron in some ways
and differs in others. A key difference is the circular passage of zinc from the
small intestine to the body and back again.
The rate of zinc absorption varies from about 15 to 40 percent, depending on
the amount of zinc consumed—as zinc intake increases, the rate of absorption decreases,
and as zinc intake decreases, the rate of absorption increases.27 Like iron,
dietary factors such as phytates influence absorption, limiting its bioavailability.28
Upon absorption into an intestinal cell, zinc has two options. Zinc may participate
in the metabolic functions of the intestinal cell itself, or it may be retained
within the intestinal cells by metallothionein until the body needs zinc. Metallothionein
plays a key role in storing and distributing zinc throughout the body.
zinc: an essential trace mineral that is part of many enzymes
and a constituent of insulin.
metalloenzymes (meh-TAL-oh-EN-zimes): enzymes that
contain one or more minerals as part of their structures.
transcription factors: proteins that bind to specific sites in
DNA and alter gene expression.
metallothionein (meh-TAL-oh-THIGH-oh-neen): a sulfurrich
protein that avidly binds with and transports metals such
as zinc.
● metallo 5 containing a metal
● thio 5 containing sulfur
● ein 5 a protein
Zinc Transport After being absorbed, some zinc eventually reaches the pancreas,
where it is incorporated into many of the digestive enzymes that the pancreas
releases into the small intestine at mealtimes. The small intestine thus receives
two doses of zinc with each meal—one from foods and the other from the zincrich
pancreatic juices. The recycling of zinc in the body from the pancreas to the
small intestine and back to the pancreas is referred to as the enteropancreatic
circulation of zinc. Each time zinc circulates through the small intestine, it may
be excreted in shed intestinal cells or reabsorbed into the body (see Figure 13-8).
The body loses zinc primarily in feces. Smaller losses occur in urine, shed skin,
hair, sweat, menstrual fluids, and semen.
Numerous proteins participate in zinc transport. Zinc's main transport vehicle
in the blood is the protein albumin. Some zinc also binds to transferrin—the
same transferrin that carries iron in the blood.
Zinc Deficiency Severe zinc deficiency is not widespread in developed countries,
but in the developing world, nearly 2 billion people are zinc deficient.29 Human
zinc deficiency was first reported in the 1960s in children and adolescent boys
in Egypt, Iran, and Turkey. Children have especially high zinc needs because
they are growing rapidly and synthesizing many zinc-containing proteins, and
the native diets among those populations were not meeting these needs. Middle
Eastern diets are traditionally low in the richest zinc source, meats. Furthermore,
the staple foods in these diets are legumes, unleavened breads, and other wholegrain
foods—all high in fiber and phytates, which inhibit zinc absorption.*
Figure 13-9 shows the severe growth retardation and mentions the immature
sexual development characteristic of zinc deficiency. In addition, zinc deficiency
hinders digestion and absorption, causing diarrhea, which worsens malnutrition
not only for zinc, but for other nutrients as well. It also impairs the immune
response, making infections likely—among them, pneumonia and GI
tract infections, which worsen malnutrition, including zinc malnutrition (a classic
downward spiral of events).30 Chronic zinc deficiency damages the central nervous system and brain and may lead to poor motor development and cognitive
performance. Because zinc deficiency directly impairs vitamin A metabolism,
vitamin A-deficiency symptoms often appear. Zinc deficiency also disturbs thyroid
function and the metabolic rate. It alters taste, causes loss of appetite, and slows
wound healing—in fact, its symptoms are so pervasive that generalized malnutrition
and sickness are more likely to be the diagnosis than simple zinc deficiency. Zinc Toxicity High doses (more than 50 milligrams) of zinc may cause vomiting,
diarrhea, headaches, exhaustion, and other symptoms. The UL for adults was set
at 40 milligrams based on zinc's interference in copper metabolism—an effect
that, in animals, leads to degeneration of the heart muscle.
Zinc Recommendations and Sources Figure 13-10 shows zinc amounts in
selected foods per serving. Zinc is highest in protein-rich foods such as shellfish
(especially oysters), meats, poultry, milk, and cheese. Legumes and whole-grain
products are good sources of zinc if eaten in large quantities; in typical US diets,
the phytate content of grains is not high enough to impair zinc absorption. Vegetables
vary in zinc content depending on the soil in which they are grown. Average
zinc intakes in the United States are slightly higher than recommendations.
Zinc Supplementation In developed countries, most people obtain enough
zinc from the diet without resorting to supplements. In developing countries,
zinc supplementation plays a major role in effectively reducing the incidence
of disease and death associated with diarrhea and pneumonia.31
Zinc lozenges may shorten the duration, but not the severity, of common
cold symptoms.32 Lozenges of zinc acetate or zinc gluconate are most effective, whereas other zinc compounds, including those with flavor enhancers, are much
less effective.33 In addition to selecting the appropriate zinc formulation, consumers
need to take relatively high doses (75 milligrams) of the lozenges within
24 hours of the onset of symptoms and continue daily throughout the duration
of the cold.34 Common side effects of zinc lozenges include nausea and bad taste
reactions.
Iodine Traces of iodine are indispensable to life. In the GI tract, iodine from
foods becomes iodide, which is readily absorbed.
Iodide Roles in the Body Iodide is an integral part of the thyroid hormones that
regulate body temperature, metabolic rate, reproduction, growth, blood cell production,
nerve and muscle function, and more.* By controlling the rate at which
the cells use oxygen, these hormones influence the amount of energy expended
during basal metabolism.
Iodine Deficiency The hypothalamus regulates thyroid hormone production by
controlling the release of the pituitary's thyroid-stimulating hormone (TSH).**
With iodine deficiency, thyroid hormone production declines, and the body responds
by secreting more TSH in a futile attempt to accelerate iodide uptake by
the thyroid gland. If a deficiency persists, the cells of the thyroid gland enlarge
to trap as much iodide as possible. Sometimes the gland enlarges until it makes a
visible lump in the neck, a goiter (shown in Figure 13-11).
Goiter aff licts about 200 million people the world over, many of them in
South America, Asia, and Africa. In all but 4 percent of these cases, the cause is
iodine deficiency. As for the 4 percent (8 million), most have goiter because they
regularly eat excessive amounts of foods that contain an antithyroid substance (goitrogen) whose effect is not counteracted by dietar y iodine. Goitrogencontaining
foods include vegetables such as cabbage, spinach, radishes, and rutabagas;
legumes such as soybeans and peanuts; and fruits such as peaches and
strawberries. The goitrogens present in plants remind us that even natural components
of foods can cause harm when eaten in excess.
Goiter may be the earliest and most obvious sign of iodine deficiency, but the
most tragic and prevalent damage occurs in the brain. Iodine deficiency is the most
common cause of preventable mental retardation and brain damage in the world.
Nearly one-third of the world's school-age children have iodine deficiency.35 Children
with even a mild iodine deficiency typically have goiters and perform poorly
in school. With sustained treatment, however, mental performance in the classroom
as well as thyroid function improves.
Even in the United States, pregnant women may not get as much iodine as
they need.36 A severe iodine deficiency during pregnancy causes the extreme and
irreversible mental and physical retardation known as cretinism.* Cretinism
affects approximately 6 million people worldwide and can be averted by the
early diagnosis and treatment of maternal iodine deficiency. A worldwide effort
to provide iodized salt to people living in iodine-deficient areas has been
dramatically successful. An estimated 70 percent of all households in developing
countries have access to iodized salt.37 Because iron deficiency is common
among people with iodine deficiency and because iron deficiency reduces the
effectiveness of iodized salt, dual fortification with both iron and iodine may be
most beneficial.
Selenium The essential mineral selenium shares some of the chemical characteristics
of the mineral sulfur. This similarity allows selenium to substitute for
sulfur in the amino acids methionine, cysteine, and cystine.
Selenium Roles in the Body Selenium is one of the body's antioxidant nutrients,
working primarily as a part of proteins—most notably, the glutathione peroxidase
enzymes.38 Glutathione peroxidase and vitamin E work in tandem. Glutathione
peroxidase prevents free-radical formation, thus blocking the chain
reaction before it begins; if free radicals do form and a chain reaction starts, vitamin
E stops it. (Highlight 11 describes free-radical formation, chain reactions,
and antioxidant action in detail.) Other selenium-containing enzymes selectively
activate or inactivate the thyroid hormones.
Selenium Deficiency Selenium deficiency is associated with Keshan disease—a
heart disease that is prevalent in regions of China where the soil and foods lack
selenium.39 Although the primary cause of this heart disease is probably a virus
or toxin, selenium deficiency appears to predispose people to it, and adequate
selenium seems to prevent it.40 Symptoms of selenium deficiency include impaired
cognition and poor immunity.41
Selenium and Cancer Limited research suggests that the antioxidant action of
selenium may protect against some types of cancers.42 Selenium supplements,
however, have not proved effective in preventing cancer and may in fact damage
DNA and cause harm.43
Selenium Recommendations and Sources Selenium is found in the soil, and
therefore in the crops grown for consumption. People living in regions with
selenium-poor soil may still get enough selenium, partly because they eat vegetables
and grains transported from other regions and partly because they eat
meats, milk, and eggs, which are reliable sources of selenium. Eating as few as
two Brazil nuts a day effectively improves selenium status. Average intakes in the
United States exceed the RDA, which is based on the amount needed to maximize
glutathione peroxidase activity.
Selenium Toxicity Because high doses of selenium are toxic, a UL has been set.
Selenium toxicity causes loss and brittleness of hair and nails, garlic breath odor,
and nervous system abnormalities.
Only "iodized salt" has had iodine added.
© Craig M. Moore
selenium (se-LEEN-ee-um): an essential trace mineral that
is part of an antioxidant enzyme.
Keshan (KESH-an or ka-SHAWN) disease: the heart
disease associated with selenium deficiency; named for
one of the provinces of China where it was first studied.
Keshan disease is characterized by heart enlargement and
insufficiency; fibrous tissue replaces the muscle tissue that
normally composes the middle layer of the walls of the heart. Deficiency Symptoms
Predisposition to heart disease
characterized by cardiac tissue becoming
fibrous (Keshan disease)
Toxicity Symptoms
Loss and brittleness of hair and nails;
skin rash, fatigue, irritability, and nervous
system disorders; garlic breath odor
Selenium
RDA
Adults: 55 μg/day
UL
Adults: 400 μg/day
Chief Functions in the Body
Defends against oxidation; regulates thyroid
hormone
Significant Sources
Seafood, meat, whole grains, fruits, and
vegetables (depending on soil content)❯ REVIEW IT
Selenium is an antioxidant nutrient that works closely with the glutathione peroxidase enzyme
and vitamin E. Selenium is found in association with protein in foods. Deficiencies are associated
with a predisposition to a type of heart abnormality known as Keshan disease. The accompanying
table provides a summary of selenium.
Chromium Chromium is an essential mineral that participates in carbohydrate
and lipid metabolism. Like iron, chromium assumes different charges. In
chromium, the Cr+++ ion is the most stable and most commonly found in foods.
Chromium Roles in the Body Chromium helps maintain glucose homeostasis by
enhancing the activity of the hormone insulin.* When chromium is lacking, a
diabetes-like condition may develop, with elevated blood glucose and impaired glucose tolerance, insulin response, and glucagon response. Some research
suggests that chromium supplements lower blood glucose or improve insulin
responses in type 2 diabetes, but findings have not been consistent.49
Chromium Recommendations and Sources Chromium is present in a variety of
foods. The best sources are unrefined foods, particularly liver, brewer's yeast,
and whole grains. The more refined foods people eat, the less chromium they
ingest.
Chromium Supplements Supplement advertisements have succeeded in convincing
consumers that they can lose fat and build muscle by taking chromium
picolinate. Whether chromium supplements (either picolinate or plain) reduce
body fat or improve muscle strength remains controversial. (Highlight 14
discusses chromium picolinate and other supplements athletes use in the hopes
of improving their performance.)
Significant Sources
Meats (especially liver), whole grains,
brewer's yeast
Deficiency Symptoms
Diabetes-like condition
Toxicity Symptoms
None reported
Chromium
AI
Men: 35 μg/day
Women: 25 μg/day
Chief Functions in the Body
Enhances insulin action and may improve
glucose tolerance Significant Sources
Meats (especially liver), whole grains,
brewer's yeast
Deficiency Symptoms
Diabetes-like condition
Toxicity Symptoms
None reported
;