The Encyclopedia Of Nutrition And Good Health - O potx

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468
oats
(Avena sativa) A common cereal GRAIN
grown in temperate regions, particularly in North
America and northern Europe. There are six
species, including common oats and cultivated red
oats, that are grown in the Americas. Oats are clas-
sified as winter and spring varieties, according to
their planting time. Only about 5 percent of the
U.S. crop is used as a food crop; most ends up as
livestock feed. An inedible, loose, pithy hull sur-
rounds the kernel, or groat, and must be removed
for human consumption.
Pure oats and pure oat
BRAN are the least
processed form of oats. Oat flakes, prepared by
steaming and flaking whole kernels, are the basis
for porridge. Oatmeal is prepared by cutting ker-
nels to small granules with a mealy texture. Con-
sumption of old-fashioned oatmeal as a
BREAKFAST
CEREAL
has declined with the increased popularity
of ready-cooked oatmeal cereals. Rolled oats, pre-
pared by crushing oats with still rollers, are used in
breakfast food, cookies, breads, and
GRANOLA,
which is a mixture of rolled oats, honey, nuts,
raisins, or dates. Milling produces oat flour. Oat
flour contains a natural

ANTIOXIDANT that increases
the stability of oat flour in storage.
Oat Bran
Oat bran is derived from an outer layer of oat ker-
nels by milling. It is a good source of
SILICON, a trace
mineral needed for healthy joints, and a form of
FIBER called beta-glucan. The fiber in oat bran is
water soluble and differs from water-insoluble
WHEAT bran, the kind usually found in bran-
enriched breakfast cereals. Eating oat bran daily in
muffins and a bowl of hot oatmeal—together with
daily exercise and eating less animal
FAT as found in
red
MEAT and BUTTER—can lower blood fat and
CHOLESTEROL even in diabetics. Oat bran alone has
a modest effect in lowering elevated levels of the
less desirable
LOW
-DENSITY LIPOPROTEIN (LDL) cho-
lesterol. Oat bran has been used as a fat substitute
to reduce fat in beef and pork sausage products. A
mixture of oatmeal and oat flour has been devel-
oped by the
USDA as a fat-substitute called Oatrim
or “hydrolyzed oat flour.” Oatrim contains one
calorie per gram, as compared with nine calories
per gram of fat and four calories per gram of
STARCH. This fat substitute is used in baked goods

and processed meats, and other products are under
development.
Oatmeal
Hot oatmeal is a traditional breakfast, and its emer-
gence as an important source of fiber has caused a
resurgence in popularity. Steel cut, rolled, or quick-
cooking oats all contain the same amount of fiber.
However, processed, cold oat breakfast cereals con-
tain much less fiber (about 2 g per serving). Dry
oatmeal contains about 14 percent protein, but
cooked oatmeal is only about 2 percent protein.
Nutrient content of regular cooked oatmeal or
rolled oats, (1 cup fortified) is: 145 calories; pro-
tein, 6 g; carbohydrate, 25.2 g; fiber, 9.23 g; fat, 2.3
g; iron, 1.6 mg; sodium, 285 mg; vitamin A, 453
retinol equivalents; thiamin, 0.53 mg; riboflavin,
0.29 mg; niacin, 5.9 mg.
obesity An excessive accumulation of body fat
for a given body size based on muscle and bone
(frame size). In 1998 the federal government
adopted new standards for determining whether a
person is overweight or obese. Before then, people
were considered overweight if their weight was
at least 10 percent to 20 percent over optimal
body weight. Obesity was defined as being more
than 25 percent over the optimal body weight for
men and 30 percent over the optimal body weight
for women.
Under the new standards, a person with a
BODY

MASS INDEX
(BMI) of 25 or more is considered over-
weight. The BMI is determined by dividing a per-
son’s weight in kilograms by the square of his or her
height in meters. A healthy BMI falls between 19
and 25. A person with a BMI of 30 or above is con-
sidered obese. According to statistics compiled by
the World Health Organization, obesity is increasing
worldwide—an estimated 1.2 billion people in the
world are overweight. Its rapid increase among
Americans during the 1990s (12 percent in 1991 to
17.9 percent in 1998) prompted some health offi-
cials to conclude that it had reached epidemic pro-
portions. In 2001 27 percent of adults between the
ages of 20 and 74 were obese. The rate of over-
weight among children was 13 percent.
Based on these figures, a former U.S. surgeon
general, David Satcher, concluded that overweight
and obesity may soon cause as much preventable
disease and death as cigarette smoking. The condi-
tions were already responsible for as many as
300,000 premature deaths each year, costing the
nation an estimated $117 billion. The prevalence
varies among groups. The average American adult
gains a pound a year through middle age.
Childhood obesity has increased dramatically
since 1965 in the United States, reflecting an
increased prevalence of obesity among children in
Western countries. The rising rate of overweight
and obesity among young people is of special con-

cern because childhood and adolescence is often a
time in life when people are the most active and
therefore least likely to gain excessive weight.
Also, unhealthy nutrition and lifestyle habits that
lead to overweight and obesity developed during
this time have a good chance of continuing into
adulthood.
The number of obese Americans has increased,
despite a national preoccupation with dieting. The
fear of being fat has become an American obses-
sion. U.S. society places a premium on being slen-
der and most women and some men have dieted at
least once. Being obese or overweight often brings
a profound social stigma affecting personal life, life
insurance premiums, and employment opportuni-
ties. Nevertheless, in the 1980s the renewed inter-
est in healthy lifestyles in America apparently
affected a limited number of people. Sedentary
lifestyles continue to prevail.
Types of Obesity
Hyperblastic obesity is characterized by an exces-
sive number of fat cells. Increased fat cell size is
classified as hypertrophic obesity, and individuals
with hyperblastic-hypertrophic obesity have
increased numbers of enlarged fat cells in their adi-
pose tissue. Hyperblastic obesity is usually associ-
ated with childhood, while hypertrophic obesity
develops later in life and is associated with diabetes
and other aspects of metabolic imbalance.
Obesity as a Health Hazard

It has been noted that the death rate increases 2
percent for each pound over a person’s healthy
weight. For persons who are 40 pounds over-
weight, the death rate is estimated to be 80 percent
higher during the next 25 years of their life. Lean
men survive longer than overweight men in the
United States. Obesity increases the risk of
HEART
DISEASE
, diabetes, GOUT, ARTHRITIS, CANCER of the
liver and esophagus,
GALLSTONES, hernia, intestinal
blockage, kidney disease, and
TOXEMIA of preg-
nancy. In the United States, obesity increases the
risk of angina, high blood pressure (
HYPERTENSION),
high blood fat, elevated (
LOW-DENSITY LIPOPROTEIN)
LDL, and sudden death from heart disease. One
clue to understanding the relationship between
obesity and elevated blood fat is the observation
that obese people have higher insulin levels, which
seems to promote higher blood lipids.
The location of fat accumulation makes a differ-
ence in health risks. Male-patterned obesity, with
fat deposited primarily in the abdomen and trunk,
is called android obesity (the “spare tire” or “apple”
profile). Android obesity in men or women is asso-
ciated with an increased risk for

CARDIOVASCULAR
DISEASE
, hypertension, elevated BLOOD SUGAR, and
gallstones. The greater the proportion of abdominal
fat, the greater the risk. Abdominal fat may be
more readily converted to cholesterol than fat
deposited elsewhere. Pear-shaped people, with fat
accumulation around the hips, do not experience
as much diabetes or high blood pressure or as many
heart attacks as those whose fat is around the
middle.
obesity 469
Possible Mechanisms
for Regulating Body Weight
Complex mechanisms involving the
NERVOUS SYS-
TEM, the ENDOCRINE SYSTEM, and the DIGESTIVE SYS
-
TEM, and adipose tissue regulate eating, energy
balance, and thus obesity. Regions of the brain, such
as the
HYPOTHALAMUS and the brain stem, help reg-
ulate food intake, body weight, body size, and body
fat content. The hypothalamus plays a critical role in
eating and balancing energy requirements with
intake. The lateral hypothalamus controls eating
activity; the paraventricular nucleus regulates nutri-
ent balance and the ventromedial hypothalamus
regulates energy balance by regulating the sympa-
thetic nervous system, which helps the body adapt

to stress. The hypothalamus regulates the
ENDOCRINE
SYSTEM
(hormone secreting system). It activates the
PITUITARY GLAND, which signals the adrenal gland to
release
GLUCOCORTICOIDS
. In turn, these STEROID hor-
mones regulate the nervous system, appetite, and
fat metabolism. Obesity is linked to altered function
of the brain stem and hypothalamus and to changes
in the autonomic nervous system, which regulates
energy expenditure and regulates thermogenesis. At
the molecular level, altered production of
NEURO-
TRANSMITTERS, chemicals required to transmit nerve
impulses, brain peptides, and brain hormones, may
alter critical control and feedback mechanisms that
maintain body weight.
Several hypotheses link food intake and energy
balance to regulate body weight through an inter-
play between the endocrine system and the ner-
vous system. A hypothetical very general control
system involves the following components: A pro-
posed “controller” resides in the brain. Signals leav-
ing the brain regulate heat production, physical
activity, food intake, energy storage as fat, and
metabolism for doing work and producing heat.
These factors stimulate the release of hormones.
Nutrients and hormones from various glands and

fat cells are then carried back to brain centers that
in turn generate signals that are interpreted by the
hypothalamus to diminish eating. Stomach disten-
sion triggers the nervous system to create a feeling
of fullness. The action of
GLUCOSE (blood sugar),
fat, and protein in the intestines on receptors could
also send signals back to the brain to diminish eat-
ing behavior.
In 2002 researchers reported that the recently
discovered “hunger hormone” ghrelin might be a
significant factor in determining why some people
become obese and why most people find it hard to
keep weight off once it is lost. A study of a small
group of obese people revealed they had much
higher blood levels of ghrelin, which is produced
by stomach cells, after they lost weight through
diet control and exercise. In contrast, people who
lost weight after gastric bypass surgery, which
reroutes the flow of food, had low levels of ghrelin.
The extremely low levels of ghrelin in people who
had undergone gastric bypass surgery might
explain why these people were usually more suc-
cessful in keeping weight off. Researchers cau-
tioned that the results were preliminary and that
ghrelin is probably only one of many tools the body
uses to regulate body weight.
Another hypothesis predicts a “set point” that
tends to keep body weight at a constant level.
According to the “set point” hypothesis for body

weight, each person has a biologically determined
body weight, believed to be inherited. In some
obese individuals, the set point may be too high.
When fat cells decrease in size (for example, after
DIETING) they could indirectly signal the brain to
increase food consumption. Thus, an obese person
with large numbers of fat cells could crave food,
leading to excessive eating after dieting. According
to a related hypothesis, some obese people earlier
in their lives, perhaps during early childhood, ate
much more than their bodies needed during their
formative years. According to this proposal, this
event patterned the body for burning energy and
storing fat. Once overweight, obesity in these indi-
viduals could be sustained even when consuming
an average amount of food.
Insulin insensitivity (resistance to the action of
insulin) correlates with obesity; increasing tissue
sensitivity to insulin is hypothesized to lower the
body’s set point. Recent discoveries shed light on
the relationships among obesity, satiety, and non-
insulin dependent diabetes. Fat cells normally
secrete a protein called
LEPTIN that induces satiety.
Leptin signals the brain to reduce consumption of
fatty foods and possibly to increase the basal
metabolism of fat cells. Therefore, leptin helps reg-
ulate body weight by limiting body fat accumula-
470 obesity
tion. Mice with mutations on the gene coding for

leptin become obese. Researchers now believe
obese people often make more than enough leptin,
but the brain does not respond effectively to shut
down eating because its binding sites or cell signal-
ing mechanisms are defective. A region of the brain
likely to be affected by leptin is the
HYPOTHALAMUS,
which integrates many functions of the body.
Specifically, the region known as ventromedial
nucleus, which regulates satiety, may be involved.
Leptin could shut off signals in the brain that direct
feeding (hunger signals), including neuropeptides.
One possibility is neuropeptide Y, which induces
lab animals to eat more carbohydrate and fat. In
the set point model, leptin could act like a ther-
mometer: When the body gets too thin, less leptin
is made, more food is eaten, and less energy is con-
sumed. When the body gets too fat, more leptin is
made, less food is consumed, and more energy is
burned.
A variety of mutations in other genes link obe-
sity and diabetes. As an example, mutations in a
protein called beta
3
-adrenergic receptor, an attach-
ment site which binds a
NEUROTRANSMITTER (norep-
inephrine), increase the risk of middle-age weight
gain and diabetes. Under normal conditions norep-
inephrine produced by the sympathetic nervous

system stimulates fat cells to burn stored fats. The
implication is that with a faulty neurotransmitter
attachment site in fat tissue, the body burns less fat
efficiently and calories accumulate. As an alterna-
tive to the set point hypothesis, the “settling point”
theory proposes that body weight is not fixed, but
that it is maintained according to feedback loops
that are determined by an interplay between genes
and environment. Systems controlling hunger and
satiety respond rapidly to dietary protein and car-
bohydrate, but the feedback from a fatty meal may
be too slow to prevent overconsumption. Thus,
increased dietary fat could alter the body’s equilib-
rium and shift body fat upward. The number of fat
cells in the body is a determining factor. Fat cells
are added during childhood and it could very well
be that how much fatty food is consumed and how
many calories are burned before adulthood has a
major impact for the risk of obesity.
Human obesity is a complex phenomenon with
many causes. Inheritance as well as diet and med-
ical history can contribute to excessive weight gain
and many questions about the detailed interrela-
tionships remain unanswered. Apparently, many
genes interact to control weight, it is therefore
unlikely that any single pharmacologic agent
related to a gene product will substitute for chang-
ing the diet and exercising regularly to maintain
desired weight. In any event, very extensive clini-
cal experience suggests that diets—that improve

insulin sensitivity and glucose tolerance by empha-
sizing
VEGETABLES and LEGUMES and minimizing
sugary or high fat foods—together with regular
physical exercise can support long-term weight loss
and reduce the risk of cardiovascular disease.
Causes of Obesity
Many adults achieve an energy balance in which
caloric intake matches energy expenditure. Body
fat does not change very much under these condi-
tions. Excessive body fat could be related to eating
more calories or to small energy expenditure, or
both. Energy expenditure refers to the calories
spent for body functions, physical activity, diges-
tion, and food metabolism. Both heredity and the
environment play a part in obesity and, therefore,
there is no single approach to treatment. Overeat-
ing, differences in metabolism,
AGING, genetic pre-
disposition, and excessive food consumption
during early childhood have been implicated.
Overeating Clearly the prolonged consump-
tion of excessive calories, when energy intake
exceeds energy expenditure, leads to obesity.
Energy expenditure refers to the calories spent for
body functions, physical activity, digestion, and
food metabolism. Body fat can be reduced only
when energy expenditure exceeds caloric intake.
The body adapts to excessive food consumption—
whether excessive

PROTEIN, CARBOHYDRATE, fat, or
ALCOHOL—by storing the surplus calories as body
fat. Many reports have suggested that obese people
eat the same, or sometimes less than nonobese
people. Using new research methods based on
ingesting double-labeled water, that is, water con-
taining a “heavy” form of oxygen (O
18
) and
“heavy” hydrogen (deuterium), investigators have
demonstrated that, on the average, obese people
generally eat more, but they habitually underre-
port their food consumption.
obesity 471
Differences in Energy Expenditure Although
obese people are generally less active than non-
obese people, they tend to use the same amounts of
energy because they weigh more. Sedentary
lifestyles contribute to obesity. About 70 percent of
adult Americans fail to exercise 20 minutes or
more three times a week as recommended. Most
people will lose weight if such an exercise program
is coupled with consuming no more than 1,500
calories daily. Individuals who exercise regularly,
or who exercise before and after a high-
calorie meal, lose more energy as heat after eating
than those who do not exercise.
Differences in Metabolism This picture is
unclear. Very rarely do glandular imbalances lead
to obesity. Cushing’s syndrome, excessive produc-

tion of glucocorticoids, a form of adrenal hormone,
is an example of hormone imbalance that can pro-
mote obesity. Obese people do not have unusually
slow metabolisms. When resting metabolic rates
are compared based upon the muscle/bone mass,
there is not a significant difference between meta-
bolic rates of nonobese and obese individuals. For-
merly obese individuals preferentially store fat
rather than burn it, and studies suggest that over-
weight and obese people tend to eat more fat and
less carbohydrate. In general, the body consumes
calories more slowly after weight is lost, and it
burns calories more rapidly when weight is gained,
for fat as well as for thin people. One hypothesis
contends that people adjust their metabolism to
maintain a “set point” weight. Thus someone who
has lost significant amounts of fat (10 percent of
their body weight) will burn fewer calories when
exercising than someone who has maintained his
or her weight without a weight-loss program.
Apparently, the body adjusts its metabolism by
altering the efficiency of muscles in burning calo-
ries. Recently, a type of prostaglandin has been
shown to act as a hormone to trigger the produc-
tion of fat cells from immature cells.
Aging In the United States, both men and
women tend to become fatter with increasing age.
This could be due to a decreased metabolic rate (a
lower
BASAL METABOLIC RATE) and a sedentary

lifestyle coupled with an easy access to high-calorie
food.
Meal Frequency The frequency of meals and
meal composition may be a factor in obesity. Eating
fewer meals may increase fat deposition, while
smaller, more frequent meals, with more food at
breakfast and less at supper, may promote weight
loss.
TV Watching Excessive TV watching correlates
with overeating. Reduced physical activity, lowered
metabolic rates, as well as visual cues to eating
high-fat snack foods and drinking alcoholic bever-
ages, contribute to the increased prevalence of
overweight. Dietary fat, which provides nine calo-
ries per gram, is more fattening than either protein
or carbohydrate, which provide four calories per
gram. Fat calories in food differ from calories in
carbohydrate: Fat in food is more easily converted
to body fat than is carbohydrate.
Inheritance One broad generalization can be
made: Obesity persists over a life span. Fat children
tend to become fat adults, suggesting a predisposi-
tion to being overweight. Early adulthood is an
important period for the development of lifelong
patterns. The question remains, to what degree is
obesity the product of genetics? Studies with twins
suggest that between 50 percent and 70 percent of
the variability in relative body weight represents
genetic variability. Current research focuses on
locating specific obesity genes. Genes influence

both metabolism and behavior. Many genes regu-
late hunger and satiety. A flurry of recent research
has yielded impartial genetic discoveries: gene OB
causes fat cells to produce a satiety protein called
lepin. A gene then codes for the receptor of this
hormone in the brain. Still another gene codes for
a hormone-producing enzyme (carboxypeptidase
E). A gene that codes for a neurotransmitter recep-
tor (binding site; Beta
3
-adrenergic receptor) for
norepinephrine is also implicated in maintaining
weight. Mutations of these genes can increase the
risk of obesity and diabetes in lab animals and pos-
sibly in people. There will be more to add to this
unfinished story as more discoveries are made.
Successful Weight Loss
A Willingness to Change Therapeutic ap-
proaches to obesity and weight management have
met with only modest success. Only 2 percent to 10
percent of Americans who diet to lose weight and
participate in weight loss programs will keep the
pounds off more than several years. Most of the lost
fat is regained within a few months after the dieter
472 obesity
discontinues the diet regimen. Dieting without a
long-term commitment to changing daily habits is
destined to fail.
Attitude is perhaps the most prominent factor in
changing behavior. Regarding overeating, under-

standing underlying feelings for which overeating
compensates seems essential for permanent weight
loss. Eating can provide immediate gratification, but
this seldom resolves deep-seated emotional issues.
After short-term sensory satisfaction, emotional
pain or longing often returns. For example,
responding to feelings of low self-esteem by crash
dieting does not solve the underlying issue, and too
often the dieter returns to old eating habits. Coun-
selors recommend beginning with an inventory of
talents and qualities that fill your life with the most
satisfaction and choosing activities and relationships
that bring satisfaction and a sense of well-being.
Slow Weight Loss Successful long-term weight
control requires the slow loss of body fat without
cyclic, on-again, off-again dieting (
YO-YO DIETING).
Losing a pound a week helps maintain muscle
(
LEAN BODY MASS) while preferentially losing fat.
Exercise Exercising for life helps keep the body
engine “revved up,” so that more calories are
burned by muscle and less insulin is required to
dispose of elevated blood sugar following meals.
Improved Diet A high-fat, high-calorie, low-
fiber diet is thought to be the major dietary factor
in obesity in the United States. Therefore the rec-
ommended diet might be low in fat, high in fiber
and complex carbohydrates (60 percent to 70 per-
cent of calories), with adequate protein (10 percent

to 15 percent of calories). Emphasis on natural,
whole foods simplifies this task of avoiding the per-
vasive high-calorie foods that fill the American
food landscape. Another approach to obesity and
overweight focuses on helping people through
advocacy and social support with the premise that
being overweight can be part of an enjoyable, ful-
filling life: The Association for the Health Enhance-
ment of Large People and the National Association
to Advance Fat Acceptance are two such groups.
Weight Loss Drugs
Like diets, anti-obesity drugs tend to be effective
only as long as the patient follows the prescription.
When drugs are withdrawn, weight lost usually
returns unless permanent behavior changes have
been made. Amphetamines have adverse side
effects: They have the potential for addiction and
tolerance (more drug is required to get the same
effect with chronic use). Another class of drug pro-
motes nutrient malabsorption so that patients tak-
ing these drugs do not absorb calories efficiently.
Two appetite suppressants, fenfluramine and
dexfenfluramine, were taken off the market by the
U.S.
FDA in 1997 when it was discovered that thou-
sands of patients who took these drugs developed
potentially deadly primary pulmonary hyperten-
sion and heart valve abnormalities. Dexfenflu-
ramine was shown to cause these injuries when
taken alone, and fenfluramine was linked to valve

problems in patients who combined it with the
drug phentermine in a mixture popularly known
as “fen-phen.” Both fenfluramine and dexfenflu-
ramine helped patients lose weight by increasing
serotonin levels in the blood stream, which pro-
vided a sense of well-being and satiety. The prob-
lem, researchers discovered after the drugs were
removed from the market, was that the drugs
destroyed the body’s ability to control the amount
of serotonin circulating in the blood. Excessive
amounts of serotonin can cause cell damage to car-
diopulmonary structures.
In late 2000 the FDA issued a public health advi-
sory warning patients about phenylpropanolamine
hydrochloride (PPA). This drug is widely used in
both over-the-counter and prescription-only nasal
decongestants and for weight control in some over-
the-counter drug products. The warning was issued
after medical researchers published a study show-
ing that phenylpropanolamine increases the risk of
hemorrhagic stroke (bleeding into the brain or into
tissue surrounding the brain) in women. Men may
also be at risk. Since then the FDA has taken steps
to remove PPA from all drug products. No drug is
both entirely safe and effective for weight loss, nor
is it certain that taking current medications for
many years is better than being fat. Drugs that sup-
press appetite are not recommended for those who
wish to lose only 5 to 10 pounds of fat.
Childhood Obesity

An estimated 13 percent of U.S. children six to 11
years old and 14 percent of adolescents 12 to 19
years old are overweight. The number of obese
children and adolescents in the United States dou-
obesity 473
bled between 1982 and 2002. Obesity is recognized
as a U.S. epidemic affecting children. Low-income
minority children face even higher rates of obesity.
An overweight adolescent between age 10 and 14
who has at least one overweight or obese parent
has a 79 percent likelihood of being overweight as
an adult.
Childhood obesity is linked to many of the fac-
tors that cause adult obesity:
Heredity As in adult obesity, genes play a role.
Children born to obese mothers are more likely to
be obese. If both parents are obese, the probability
of their children becoming obese is very high.
Overfeeding Some babies have more fat cells
than usual. If they are also overfed, they are more
likely to become obese children. In addition, over-
feeding a child may lead to larger, not more, fat
cells. This may make controlling weight more diffi-
cult as an adult. (It should be pointed out that
plump babies do not necessarily become obese
adults.)
Lower Metabolism Infants who become over-
weight during their first year have a lower basal
metabolic rate than usual. Their mechanism for reg-
ulating body weight might be lower than average.

Eating Too Much Fatty Food The more
JUNK
FOOD
is consumed, the more likely the child will be
obese. Bogalusa Heart Study is an ongoing popula-
tion study to examine risk factors for cardiovascu-
lar disease in children. Results from this study
reveal that children who consume more than 30
percent of their calories from fat were more likely
to eat less
CALCIUM, IRON, MAGNESIUM, and vitamins
like
RIBOFLAVIN, NIACIN, THIAMIN, VITAMIN B
6
, VITA-
MIN B
12
, and VITAMIN E.
Too Much TV and Not Enough Exercise The
odds of becoming obese increase with the number
of hours of TV viewed each day. Children’s basal
metabolic rate decreases, and they get less physical
activity. Children who watch TV eat more of the
high-calorie, highly processed food they see adver-
tised, and parents fill the role of food “gate keepers.”
Children eat what is available to them, whether it is
candy, soft drinks, or fatty convenience foods, or
fruit, low-fat foods, and sugar-free beverages.
The home environment and parents present the
model for a child’s eating habits. A child’s shift to a

more healthful lifestyle needs to be nurtured by
parents to become permanent. As with overweight
adults, regular exercise is extremely important in
children’s health and maintaining a desirable
weight.
However, overzealous dietary restrictions by
parents can encourage self-imposed dieting and
eating disorders, a prevalent problem among chil-
dren and adolescents in the United States. As many
as 80 percent of 10-year-old girls suffer from a fear
of body fat; some already show signs of dieting,
bingeing, overeating, and anorexia. The message
they are receiving is that any accumulation of body
fat is socially unacceptable. However, among
white, middle-class, healthy girls in the United
States, weight before and during puberty does not
seem to be a predictor of weight gain at middle age.
On the other hand, weight gained after puberty
(during early adolescence) has correlated with
weight gain as adults. For boys, prepuberty weight
appears to be a good predictor of adult obesity. A
physician should be consulted before talking to
children about weight. Periodic increases in fat,
especially among girls, are a normal occurrence.
Weight maintenance, after the child has grown into
his or her own weight, is preferable to dieting.
Generally, children can be taught to prefer lower
fat foods by exposure and availability. (See also
MALNUTRITION; WEIGHT MANAGEMENT
.)

Asayama, Kohtaro et al. “Increased Serum Cholesterol
Ester Transfer Protein in Obese Children,” Obesity
Research 10 (2002): 439–446.
Cummings, D. E. et al. “Plasma Ghrelin Levels After Diet-
Induced Weight Loss or Gastric Bypass Surgery,” New
England Journal of Medicine 346, no. 21 (May 23,
2002): 1,623–1,630.
octacosanol A complex alcohol that is a normal
constituent of wheat germ and wheat germ oil.
Other sources include whole grain cereals, seeds
and
NUTS, and many plant oils and WAXES. Persis-
tent claims that octacosanol supplementation has a
positive effect on physical endurance and muscular
strength have not been substantiated by research.
The Federal Trade Commission concluded that
wheat germ oil did not improve endurance or sta-
mina. Octacosanol seems to improve reaction time.
(See also
ERGOGENIC SUPPLEMENTS.)
oil See VEGETABLE OIL.
474 octacosanol
oil palm (Elaeis guineensis) A palm that is a
major source of edible oil. The oil palm yields more
oil per acre than any other plant. It originated in
West Africa, and plantations now exist in Malaysia,
China, and Indonesia, as well as Tanzania, the
Ivory Coast, Nigeria, and other regions. Palm oil is
prepared from fibrous pulp of the fruit, and palm
kernel oil is obtained from the seed or kernel,

which contains about 50 percent oil. Palm kernel
oil is used for margarine production and food man-
ufacture. It is among the most
SATURATED FATS
, con-
taining 86.7 percent saturated
FATTY ACIDS
, 1.6
percent polyunsaturated fatty acids, and 11.7 per-
cent monounsaturated fatty acids. (See also
COCONUT OIL; TROPICAL OILS.)
okra
(Hibiscus esculentus; Abelmoschus esculen-
tus) A vegetable that bears seeds in edible pods
whose ancestors may have been widely distributed
from Africa to India. Okra now grows in regions
with a moderate climate, including the southern
states of the United States. Much of the U.S. okra
crop is frozen or canned. Okra contains a mucilage
that acts as a thickener in soups and stews. Because
okra changes to an unappetizing color when
cooked in utensils containing iron, copper, or brass,
glass or stainless steel containers are used. Okra’s
slippery mucilage is balanced by acidic foods like
tomatoes and lemons and by vinegar. Okra, long
considered part of Deep South cuisine, is also part
of Indian, Caribbean, South American, and African
recipes.
Nutrient content of okra (8 pods, 85 g, cooked)
is: 27 calories; protein, 1.6 g; carbohydrate, 6.1 g;

fiber, 2.75 g; calcium, 54 g; iron, 0.38 mg; potas-
sium, 274 mg; vitamin C, 14 mg; thiamin, 0.11 mg;
riboflavin, 0.05 mg; niacin, 0.74 mg.
oleic acid A nonessential FATTY ACID and a com-
mon constituent of
FATS and OILS found in foods
and fat synthesized by the body. Oleic acid is dis-
tinguished from the other common fatty acids, the
energy-rich building blocks of fats and oils. It con-
tains 18 carbon atoms and a single double bond, is
deficient in hydrogen atoms, and thus is classified
as a monounsaturated fatty acid. In contrast, satu-
rated fatty acids are building blocks filled up with
hydrogen atoms and polyunsaturated fatty acids
possessing two or more double bonds and are more
unsaturated than oleic acid. Oils rich in oleic acid
are called monounsaturated oils.
VEGETABLE OILS
like olive oil,
AVOCADO oil, and CANOLA OIL contain
high amounts of oleic acid. Oleic acid-rich veg-
etable oils seem to lower the less desirable forms of
blood
CHOLESTEROL, LOW-DENSITY LIPOPROTEIN (LDL)
with high fat intake, and to increase more desirable
forms of cholesterol,
HIGH-DENSITY LIPOPROTEIN
(HDL). Olive oil is more stable to oxidation than
polyunsaturates such as safflower oil or corn oil.
The recommendation is to decrease fat and oil con-

sumption generally, and to use more monounsatu-
rates in cooking, rather than saturates (butter, lard,
shortening, coconut oil, or palm oil) or polyunsat-
urates (such as
CORN OIL, SAFFLOWER oil, and SOY-
BEAN oil).
Olestra (sucrose polyester, imitation fat [Olean])
A noncaloric fat substitute approved for use in
snack foods such as crackers, potato chips, and
other chips. Olestra tastes like
LARD and VEGETABLE
OILS
; it is neither digested nor absorbed by the
body. By comparison,
FAT and oils contain 126 calo-
ries per tablespoon. Olestra resembles the structure
of fat, except that it has a molecule of sucrose at its
core to which are attached eight fatty acids, rather
than three. Because it possesses a new substance,
sucrose polyester had to be approved by the U.S.
FDA
. All products containing Olestra are labeled to
notify the consumer that Olestra may cause
abdominal cramping and loose stools and that it
inhibits the uptake of certain nutrients. Vitamins A,
D, E, and K have been added. The question of mal-
absorption of
CAROTENOIDS has not been addressed.
In addition to these potential safety problems,
animal studies suggest Olestra can cause liver dam-

age, birth defects, and cancer. More complete stud-
ies are needed to establish its safety. Regardless of
their source, fat substitutes cannot replace the need
to eat less high-fat food and to change eating
habits. (See also
WEIGHT MANAGEMENT.)
olive (Olea europaea) The oil-rich fruit of a
semitropical evergreen adapted to hot, dry cli-
mates. Olives were probably first cultivated in the
Eastern Mediterranean region as early as 6000
B.C.
There are now more than 60 varieties. Mediterran-
olive 475
ean countries remain major producers; together,
Italy and Spain produce more than half of the
world’s olives and 60 percent of the world’s olive
oil production. Olives are also grown in Australia,
China, Greece, Turkey, and France, as well as in the
United States. Spanish colonists introduced olives
to California in the 18th century; that state contin-
ues to be a major domestic supplier. At maturity,
ripened olives contain 15 percent to 35 percent oil,
and
OLIVE OIL is a major cooking oil. The oil content
varies according to soil conditions, climate, and
time of harvest.
Olives must be processed for consumption. In
the Spanish method, green (unripe) olives are first
treated with alkali, then fermented, and canned or
bottled. The alkali destroys a bitter constituent

called oleuropein. In the American method, half-
ripe, reddish fruit are cured in lye (strong alkali).
Olives darken as pigments oxidize. They are rinsed
and then placed in fermentation tanks containing
BRINE. In the Greek method, fully mature olives are
harvested and soaked in brine to remove the bitter
components. Ripe, pitted olives (10.47 g) provide
50 calories; protein, 0.4 g; carbohydrate, 2.9 g;
fiber, 1.4 g; fat, 4.5 g; calcium, 42 mg; iron, 1.5 mg;
sodium, 410 mg; and traces of B vitamins.
olive leaf extract The extracted juice of the leaf of
the olive tree. This substance has been used for cen-
turies as an herbal remedy for a variety of ailments,
especially infection and fever. In the mid-1800s Dr.
Daniel Hanbury reported that olive leaf extract was
effective in reducing fever associated with an epi-
demic of malaria on a Mediterranean island.
In recent decades researchers have discovered
that eleuropein, an ingredient in olive leaf extract,
has antibacterial, antiviral, and anti-inflammatory
properties and may help reduce the risk of
CORO-
NARY ARTERY DISEASE by lowering LOW-DENSITY
LIPOPROTEIN
(LDL) CHOLESTEROL. Laboratory studies
conducted in the 1960s revealed than an active
ingredient in eleuropein (elenolic acid) either
killed or inhibited the growth of a number of path-
ogenic organisms, including bacteria, yeasts, and
viruses, but because the compound rapidly binds to

proteins in the blood, rendering it ineffective,
attempts to develop a marketable drug from the
substance were abandoned.
There is limited clinical evidence suggesting that
olive leaf may help lower high blood pressure.
However, reliable clinical studies on human beings
that confirm the safety and potential health bene-
fits of olive leaf extract do not yet exist. Neverthe-
less, nonscientific literature is filled with anecdotal
accounts of the extract’s ability to heal. It has been
available as a dietary supplement in the United
States since the mid-1990s.
Ruiz-Gutierrez, V. et al. “Oleuropein on Lipid and Fatty
Acid Composition of Rat Heart.” Nutrition Research 15,
no. 1 (1995): 37–51.
olive oil An oil extracted from ground olives.
Spain is currently the world’s leading producer of
bulk olive oil; Italy is a leading producer of bottled
olive oil. The International Oil Agreement was
negotiated through the U.N. to ensure olive culti-
vation and olive oil production in the Mediter-
ranean region.
To produce olive oil, crushed olives are mechan-
ically pressed several times. The temperature for
olive oil extraction can be 50° to 110° F. There is no
legal definition of “cold-pressed” oil, but the hotter
the pressing, the more oil is extracted.
Olive oil is classified as a monounsaturated fat
because it contains large amounts of
OLEIC ACID,a

monounsaturated
FATTY ACID
with one double bond
and lacking two hydrogen atoms—in contrast with
polyunsaturates, containing polyunsaturated fatty
acids with two or more double bonds and lacking
several pairs of hydrogen atoms, and saturates,
containing predominantly saturated fatty acids (no
double bonds and completely filled up with hydro-
gen atoms). Because olive oil is more stable to oxi-
dation and rancidity, olive oil is not chemically
stabilized (partially hydrogenated). Olive oil, like
all oils, provides 14 g of fat per tablespoon, equiva-
lent to 120 calories.
Proposed Grades of Oil
An independent U.S.
FDA analysis of 30 imported
olive oils revealed that five were not olive oil and
18 were mislabeled as “extra virgin” oil.
“Extra virgin olive oil” is prepared from
mechanical pressing and is filtered without refin-
ing. “Virgin olive oil” is not highly refined and has
a golden color and a unique flavor and taste. The
476 olive leaf extract
acid content is no more than 1 percent. Virgin olive
oil is filtered after pressing and is unrefined; the oil
has a rather fruity flavor, and its acid content is less
than 2 percent. Oil labeled “olive oil” is usually
listed as being “100 percent pure.” It is actually a
blend of refined and unrefined olive oil and

accounts for about 70 percent of U.S. olive oil con-
sumption. Refining involves extraction at high
temperatures and with solvents, neutralization of
acids, and bleaching.
Potential Health Benefits of Olive Oil
People who eat predominantly olive oil have
lower blood fat and cholesterol and a reduced risk
of clogged arteries. Olive oil seems to lower blood
levels of the less desirable form of
CHOLESTEROL,
LOW-DENSITY LIPOPROTEIN (LDL), while raising the
level of
HIGH-DENSITY LIPOPROTEIN (HDL), the more
desirable kind of cholesterol. If the intake of
polyunsaturates increases substantially above 7
percent of daily calories, the current average,
polyunsaturated oils lower LDL (a desirable effect)
but also lower HDL (an undesirable effect). By fol-
lowing current dietary guidelines that call for eat-
ing less fat (less than 30 percent of total calories)
and less saturated fat (less than 10 percent of calo-
ries), people necessarily increase their consump-
tion of unsaturates. Substituting monounsaturated
oils for saturates and polyunsaturated fats and oils
may be desirable while decreasing total fat con-
sumption because high consumption of polyunsat-
urates is more likely to promote the oxidation of
LDL cholesterol, the less desirable form, thus
increasing the probability that oxidized LDL will be
taken up by blood vessels and create plaque in

arteries. Furthermore, animal studies suggest
polyunsaturates can increase the risk of some
forms of cancer. Cooking with olive oil instead of
polyunsaturated vegetable oils (safflower oil, corn
oil, etc.) may be advantageous because olive oil
does not break down as readily when heated. (See
also
ATHEROSCLEROSIS; CARDIOVASCULAR DISEASE;
FAT METABOLISM.)
“Special report: olive oil,” UC Berkeley Wellness Letter, 11,
no. 9 (June, 1995): 6.
omega-3 fatty acids See ESSENTIAL FATTY ACIDS;
FLAXSEED OIL.
omega-6 fatty acids See ESSENTIAL FATTY ACIDS.
onion (Allium cepa) A vegetable with an under-
ground bulb closely related to
GARLIC and leeks,
belonging to the lily family. Onions apparently
originated in prehistoric central Asia, and were
grown in ancient Egypt, Greece, and Rome, as well
as China. There are more than 500 varieties; all of
the edible species possess a pungent bulb. Euro-
peans introduced onions to the Americas. Today,
China, the United States, and India produce the
largest yields, and onions rank sixth among veg-
etable crops worldwide.
Green onions may be harvested before the onion
has matured. Alternatively, mature onion bulbs can
be harvested. The length of time that dried bulbs
can be stored ranges from several days to months,

depending on the variety, their stage of maturity,
and temperature and humidity during storage.
There are two types of dry onion. Flat onions,
elongated Spanish onions, and Bermuda onions
are usually mild flavored. They do not store as well
as globe or late-crop onions, which frequently pos-
sess a stronger flavor. The latter store well and can
be marketed throughout the year. Onions can be
canned, dehydrated, frozen, or pickled.
Onions and their relatives possess a complex
family of sulfur compounds related to the sulfur-
containing amino acid cysteine. Once their layers
are cut, the sulfur-containing compounds come
into contact with an enzyme called allinase that
releases volatile (gaseous) compounds that can irri-
tate eyes. Cooking onions and
GARLIC modifies
these sulfur compounds, and they are not so irri-
tating after cooking.
The medicinal properties of onions and garlic
have been known for thousands of years, and
recorded use includes treatment of wounds and
infections, tumors, worms and parasites, weakness,
FATIGUE, and asthma. Onions resemble garlic in
terms of active ingredients and therapeutic effects.
The consumption of garlic and onions correlates
with lowered blood cholesterol levels. Generally,
the higher the dose of garlic and onions, the greater
the reduction. Onions also seem to lower blood
CHOLESTEROL by helping to block cholesterol syn-

thesis. Onions and garlic contain a variety of pun-
gent, sulfur-containing compounds. One of these
onion 477
lowers BLOOD SUGAR; another counteracts blood
platelet stickiness and reduces the tendency for
blood to clot and, at the same time, raises
HIGH-
DENSITY LIPOPROTEIN
(HDL), the desirable form of
cholesterol that protects against cardiovascular dis-
ease. Onions help decrease elevated blood sugar
levels in diabetics, possibly by slowing the break-
down of insulin, the hormone responsible for stim-
ulating sugar uptake from the blood. They may also
increase insulin secretion.
Onions as well as garlic contain compounds
that block the production of inflammatory agents.
For example, onions contain a
FLAVONOID called
QUERCETIN
, a plant pigment known to reduce
INFLAMMATION.
Both onions and garlic have antibiotic properties
and have been shown to be effective against fungi
and parasites as well. Furthermore, onions and gar-
lic contain substances that block tumor growth in
animals. Sulfur compounds apparently induce
enzyme systems in the
LIVER that detoxify poten-
tially harmful compounds. Flavonoids are

ANTIOXI-
DANTS that block damage due to free radical attack.
Free radicals are highly reactive molecules that
avidly attack cells. Flavonoids play a role in the
anticancer properties of onions and garlic because
free radical damage is linked to cancer.
Raw, chopped onions (1 cup, 160 g) provide 54
calories; protein, 1.9 g; carbohydrate, 11.7 g; fiber,
2.64 g; iron, 0.59 mg; potassium, 248 mg; vitamin
C, 13 mg; thiamin, 0.1 mg; riboflavin, 0.02 mg; and
niacin, 0.16 mg. (See also
CARCINOGEN; HEART
ATTACK
.)
orange
(Citrus sinensis) An orange-colored CIT-
RUS FRUIT, that is the most popular fruit crop in the
United States. Orange trees grow in semi-tropical
regions and probably originated in Southeast Asia
and Southern China. Spanish explorers and
colonists brought the orange to the New World in
the 16th century. In the United States, oranges are
cultivated in Arizona, California, Texas, and
Florida.
The three principal varieties of orange include
the sweet (common, China orange), C. sinensis; the
loose-skinned orange, C. mobilis; and the sour, bit-
ter Seville orange, C. aurantium. Sweet oranges are
represented by the blood orange, the navel orange
and the Valencia (Spanish) orange, in addition to

the Hamlin, Jaffa, and Pineapple varieties. Only
sweet oranges are grown commercially in the
United States.
The color of the orange peel does not necessar-
ily indicate maturity because most oranges are
picked green and exposed to ethylene gas at warm
temperatures to enhance the orange color. Sour
oranges, such as the Seville, are grown in Spain for
marmalade and orange liqueurs.
Three quarters of U.S. orange production is
processed and 80 percent of this ends up as frozen
orange juice concentrate. Oranges and orange juice
contain large amounts of
VITAMIN C, and this con-
tributes a substantial percentage of the vitamin C
intake in the typical U.S. diet. The white inner por-
tion of the peel is a good source of
FLAVONOIDS,
plant substances that act as antioxidants to prevent
oxidative damage.
Certain individuals may be allergic to compo-
nents in the orange peel and neither the peel nor
products made from it should be eaten by such
people. Citrus peel also contains citral, a compound
that blocks the action of vitamin A. Organic orange
peels have not been sprayed with pesticides. One
orange (131 g) provides 60 calories; protein, 1.2 g;
carbohydrate, 15.4 g; fiber, 2.97 g; potassium, 237
mg; vitamin C, 70 mg; thiamin 0.11 mg; riboflavin,
0.05 mg; and niacin, 0.37 mg.

Orange Juice
Fifteen percent of the U.S. orange crop is used for
fresh orange juice. Commercial orange juice may
contain up to 10 percent mandarin orange juice
and up to 5 percent sour orange juice. Frozen
orange juice concentrate contains up to four times
higher concentrations of nutrients than fresh juice.
Orange juice can be used to enhance the flavor of
root vegetables and can be added to jams and mar-
malades. Orange juice is a good source of vitamin C
and
POTASSIUM. Most 100 percent orange juices
provide 60 mg of vitamin C or more and 80 to 100
calories per cup. The current
REFERENCE DAILY
INTAKE
(formerly the USRDA) for vitamin C is 60 mg.
Vitamin C is readily oxidized upon exposure to the
air to an inactive form. Fresh-squeezed orange
juice loses 60 percent of its vitamin C when stored
for 24 hours at room temperature, or 20 percent
when orange juice is refrigerated.
478 orange
Once prepared, orange juice should be kept
chilled in a sealed container to reduce loss of vita-
min C. In comparison with fresh orange juice,
canned orange juice has been heated, reducing the
levels of vitamin C. Up to 10 percent of U.S. frozen
orange juice concentrate was estimated to be adul-
terated with sugar, orange solids, or chemical

extenders in 1993. Some of the modifications have
been subtle and difficult to detect. One cup of
freshly squeezed orange juice provides 111 calo-
ries; 1.7 g protein; carbohydrate, 25.8 g; fiber, 0.5 g;
potassium, 496 mg; vitamin C, 124 mg; thiamin,
0.22 mg; riboflavin, 0.07 mg; niacin, 0.78 mg.
Orange Drinks
Orange drinks and sodas are not orange juice. Their
orange color is due to
ARTIFICIAL FOOD COLORS. They
represent empty calories because they are usually
low in vitamin C and potassium and contain added
SUCROSE, high FRUCTOSE CORN SYRUP, or ASPARTAME
as SWEETENERS.
oregano (Origanum vulgare; wild marjoram) An
herb used in cooking. The flavor of oregano’s dark-
green leaves resembles that of
THYME and sweet
MARJORAM, but is more pungent. The dried herb
possesses a stronger flavor than fresh leaves.
Oregano is often used to season Mexican and Ital-
ian dishes (
PASTA and PIZZA), beans, meat such as
lamb or poultry, and tomato soups. Before refriger-
ation, oregano was used to retard food spoilage.
The essential oils of oregano possess a wide range
of antifungal and bacterial activities.
organelle A subcellular particle or membrane
component within cells that possesses a specialized
metabolic function. Examples include

MITOCHON-
DRIA, the nucleus, LYSOSOMES, and ENDOPLASMIC
RETICULUM
.
Each type of cell, with the exception of
RED
BLOOD CELLS
, contains up to several hundred small,
bean-shaped structures known as mitochondria.
They are about the size of bacteria and contain
their own
DNA and protein synthesizing machinery.
Mitochondria are called the powerhouses of the
cell because they provide the enzymes that convert
fuels such as
FAT and CARBOHYDRATE to ENERGY,
yielding metabolic end products,
WATER, and CAR-
BON DIOXIDE. In the typical cell, mitochondria pro-
duce more than 90 percent of the cell’s chemical
energy in the form of
ATP.
Most cells, except red blood cells, contain a
nucleus that houses DNA, the genetic blueprint of
the cell, together with the machinery for synthesiz-
ing (replicating) DNA. The nucleus also contains
enzymes needed to repair damage to DNA. DNA
directs the formation of
RNA molecules, which
guide protein synthesis in the cytoplasm.

Lysosomes function as the cell’s garbage dis-
posal units. They degrade worn-out, damaged
structures and
PROTEIN whose components will be
recycled. Endoplasmic reticulum is a complex
membrane that houses enzymes that deactivate
drugs and chemicals; that activate the B vitamin
FOLIC ACID; elongate fatty acids; and synthesize spe-
cialized products for secretion, like digestive
enzymes of the
PANCREAS. (See also DNA; GENE;
LIVER; METABOLISM.)
organic foods Foods that have been grown with-
out chemical fertilizers and synthetic
PESTICIDES.In
the case of
MEAT and dairy products, organic refers
to animals raised without the use of growth pro-
moters like hormones, antibiotics, and other sub-
stances that are added to animal feed. Any
packaging or processing has been carried out with-
out the use of synthetic compounds.
In 1990, the U.S. Congress passed the Organic
Foods Production Act. This law required the U.S.
Secretary of Agriculture to develop a National
Organic Program (NOP), administered by the
AGRI-
CULTURAL MARKETING SERVICE, to establish uniform
standards of organic food production as well as
organic farming management. A 15-member

National Organic Standards Board (NOSB) advises
the Secretary of Agriculture on all aspects of the
NOP and creates a list of approved and prohibited
substances and ingredients in organic food produc-
tion and handling. Among the substances prohib-
ited: ash from manure burning, arsenic, lead salts,
sodium fluoaluminate (mined), strychnine, and
tobacco dust. As of October 21, 2002, organic farm-
ers and organic food handlers seeking to be recog-
nized as “organic” and to use the “organic” label
must meet national standards through certification
procedures.
organic foods 479
Organic farming emphasizes animal manure,
cultivation of legumes (plants that add nitrogen
back to the soil), and biological pest control. A
product can be “certified organic” if it contains at
least 95 percent organic ingredients. The manufac-
turer needs to list the percentage of organic ingre-
dients on the food label, or on the information
panel, unless the food is 100 percent organic.
Labeling is voluntary; food producers who meet
the government standards do not have to include
the word organic on their products, but if they
do, the labeling must meet certain requirements.
Single-ingredient foods, such as pieces of fruit, will
display a small “USDA organic” sticker. The seal also
appears on packages of meat, cartons of milk or
eggs, and cheese. Products that include organic
ingredients, such as

BREAKFAST CEREAL, fall into one
of four categories. Those with 100 percent organic
ingredients can include a statement saying that on
the front of the package as well as the “USDA
organic” seal. Products that are at least 95 percent
organic can display the seal on the package front. If
only 70 percent of the ingredients are organic, the
package may indicate the product is “made with”
the organic ingredients, and these must be listed on
the side panel. Products with less than 70 percent
organic ingredients cannot make any “organic”
claims on the front of the package, but may list
organic ingredients on the side. The Organic Food
Production Act outlines uniform national certifica-
tion criteria for organic growers and producers. This
plan requires the accreditation of individual organic
certifiers, to be defined by the NOSB. There are
about 50 certification agencies in the United States
and Canada, including the
CALIFORNIA CERTIFIED
ORGANIC FARMERS
(CCOF) and Quality Certification
Services.
Organic foods may be more costly, depending on
the season, because more hand labor is involved
when synthetic pesticides are omitted, and organic
farming carries greater business risks. Organic food
may not look as attractive as nonorganic produce
because some chemicals that create a cosmetic
effect have not been used. Nutrient-depleted soils

will produce crops with decreased levels of trace
nutrients, and good soils increase the nutritional
quality of produce. There is evidence that organic
produce may be more nutritious than produce
from conventional farms, in terms of boron, cal-
cium, chromium, copper, iodine, iron, magnesium,
manganese, potassium, silicon, selenium, and zinc.
For example, comparisons of trace minerals in
organic and conventionally grown apples, corn,
peas, potatoes, and wheat purchased over a two-
year period suggested that the average nutrient
content of organic foods can average twofold
greater than that of conventional commercial pro-
duce. One explanation is that synthetic fertilizers of
nitrate, phosphates, and other minerals do not
enrich soils with a broad spectrum of nutrient min-
erals. Commercially grown food contained more
aluminum, lead, and mercury.
Organic farming provides environmental divi-
dends as well. It requires less energy, minimizes
groundwater pollution, and reduces soil erosion.
Manure benefits the soil by building loam and
increasing water holding capacity. Legumes
increase soil nitrogen for crops. Farm worker safety
is also a consideration because synthetic pesticides
pose the greatest risk to farm workers. The high
crop yields of modern agriculture result partially
from the use of chemical fertilizers and synthetic
pesticides. The tonnage of pesticides applied to U.S.
farms has grown 33-fold since World War II, and

pesticide toxicity has increased tenfold. The
decreased use of synthetic pesticides, together with
crop rotation and biological pest control, in combi-
nation with organic farming methods and judicious
use of certain synthetic pesticides and fertilizers
and conservation, seems a realistic approach to
preserve resources.
The organic food market is growing rapidly.
According to the
AGRICULTURAL RESEARCH SERVICE,
one in four Americans buys organic foods. Retail
sales of organic products, which reached $7.8 bil-
lion in 2000, increased by 20 percent annually
between 1995 and 2001. (See also
CERTIFIED
ORGANIC VEGETABLES
; NATURAL FOOD.)
Brown, James E. Organic Gardening, Vegetable Growing in
Simple Terms. New York: Simon & Schuster, 1999.
organic meat MEAT grown without growth pro-
moters like hormones, antibiotics, and other sub-
stances that are added to animal feed. (See also
ANTIBIOTIC-RESISTANT BACTERIA IN FOOD; ORGANIC
FOODS
.)
480 organic meat
organ meat MEAT that represents internal organs
such as the
LIVER, kidney, heart, and brains. In con-
trast, nonorgan meat is comprised primarily of

muscle and connective tissue. Sweetbreads are
derived from the thymus gland of young cattle.
(See also
PROCESSED FOOD.)
ornithine A nonessential
AMINO ACID required
in the formation of
UREA, the end product of
PROTEIN
metabolism. Ornithine is made by the
body. Although not incorporated into proteins,
ornithine helps the
LIVER convert the toxic
nitrogen waste
AMMONIA to urea via the UREA
CYCLE
, the enzyme system responsible for urea
formation. Urea is eliminated by the
KIDNEYS
in urine. Ornithine is converted by the body to
ARGININE, an amino acid that functions as a pro-
tein building block. Ornithine also forms
polyamines, a family of nitrogen-containing
chemicals that play a role in cell differentiation
and growth.
Ornithine Supplements
Ornithine, as well as arginine, has found its way
into health food stores. Body builders and athletes
use ornithine out of the belief that it stimulates the
production of

GROWTH HORMONE.
Growth hormone causes muscle growth in nor-
mal animals. Moderate amounts of arginine and
ornithine do not seem to affect growth hormone
levels. Very large oral doses of ornithine may stim-
ulate the release of growth hormone; however, the
evidence that it can selectively burn fat and build
muscle remains skimpy. Ornithine’s beneficial
effects for athletes may be partially due to its role
in eliminating nitrogen waste products. In addition,
in lab animals ornithine seems to stimulate the
THYMUS GLAND, thus boosting immunity. Consump-
tion of large amounts of single amino acids over
time may cause potentially dangerous side effects.
Seizures have been reported to occur with high
doses of ornithine, and the long-term effects of a
high dosage of ornithine are not known. Ornithine
supplements are not recommended for patients
with kidney or liver conditions. Safety data are
inadequate for pregnant and breast-feeding
women. (See also
AMINO ACID METABOLISM; EXER-
CISE; LYSINE.)
orthomolecular medicine The use of NUTRIENTS
and naturally occurring materials to treat illness
and disease due to inherited enzyme deficiencies.
Human nutrition has moved beyond treating dis-
ease to preventing illness and improving the qual-
ity of life and using large amounts of
VITAMINS.

Megavitamin therapy is one strategy to treat defi-
ciencies that are the result of increased needs due
to inheritance, though it continues to be contro-
versial. The basis for this approach is the variability
in enzyme levels and efficiencies among individu-
als. Mutant enzymes can require much larger
amounts of vitamins than usual in order to func-
tion optimally. Vitamin and mineral therapy has
successfully been used to treat disease and to
improve health in some cases. Furthermore, evi-
dence points to a biochemical imbalance in neuro-
logical disorders and learning disabilities, among
others.
There is a growing awareness that mild deficien-
cies of minerals and vitamins play a role in chronic
diseases. Deficiencies of antioxidant vitamins are
linked to
CARDIOVASCULAR DISEASE and certain
forms of
CANCER, for example. Nutrient malabsorp-
tion can lead to deficiencies with aging and thera-
peutic doses of vitamins and minerals may be
required to prevent such common conditions as
osteoporosis. Environmental stress in the form of
air pollutants, drugs, viral infections, and reliance
on convenience foods increases vitamin needs, and
supplementation can be an effective strategy in
these situations.
Conditions where large amounts of vitamins
(more than 10 times the Recommended Dietary

Allowance) are well recognized clinically include
treatment of elevated cholesterol with B vitamin
niacin, and of skin disorders with vitamin A deriv-
atives. On the other hand, the use of vitamins to
treat conditions other than well-established defi-
ciency diseases is still considered unorthodox in
some medical circles.
Megavitamin treatment is not always effective.
The literature on megavitamin therapy also con-
tains exaggerated claims of cure based on misinter-
pretations of data from case studies of treated
individuals. Vitamins are generally safer than most
synthetic drugs and they are less expensive, but
most experts believe that supplements are no sub-
orthomolecular medicine 481
stitute for a wholesome diet. Excessive amounts of
any nutrient can lead to possible side effects and
toxicity. (See also
MALABSORPTION.)
Challem, J. “Beta-Carotene and Other Carotenoids:
Promises, Failures, and a New Vision,” Journal of
Orthomolecular Medicine 12 (1997): 11–19.
ossification The process of bone formation. Ossi-
fication requires
CALCIUM,
MAGNESIUM, and PHOS-
PHORUS as primary building blocks. Many trace
nutrients are needed for bone building:
MAN-
GANESE

, BORON, VITAMIN D
, VITAMIN K, VITAMIN C,
VITAMIN A, FLUORIDE, COPPER, ZINC, and SILICON. The
rate of bone growth is controlled by hormones such
as
GROWTH HORMONE from the PITUITARY GLAND and
steroid hormones produced by the ovaries and
testes. The growth of the
SKELETON requires
increased intake of calcium over the amount lost
(positive calcium balance) until adult size is
reached, usually by the late teens or early twenties.
Lengthwise bone growth in women is generally
completed earlier than in men.
Osteoblasts are cells that form calcified deposits
to make up bony structure. They secrete the con-
nective tissue protein
COLLAGEN, which forms fila-
ments that in turn form a matrix. Osteoblasts
connect with another type of cell called osteocytes,
which are bone cells that are surrounded by crys-
tallized minerals and lie deep within bone. Thus,
osteocytes and osteoblasts remain connected with
each other and maintain bone structure. Through-
out life, bone is constantly being reabsorbed and
reformed. Adult bone replacement amounts to
about 18 percent per year. (See also
OSTEOMALACIA;
OSTEOPOROSIS
; RICKETS.)

osteoarthritis A chronic, degenerative joint dis-
ease and the most common form of
ARTHRITIS. Car-
tilage may be destroyed and bone spur formation
can limit joint function. Weight-bearing joints such
as ankles, hips, spine, and knees are often affected.
A point is reached at which repair mechanisms can
no longer keep up with wear and tear. Joints may
be stiff and sore due to damage through prolonged
usage. Most Americans over the age of 50 experi-
ence a degree of osteoarthritis. Osteoarthritis may
follow infections or joint injury.
STRESS, excessive
weight, poor posture, imbalanced musculoskeletal
system, even poor muscle tone aggravate the con-
dition. Physical therapy, structural alignments and
exercise may aid in treating early degenerative
joint disease.
It is important to curtail
INFLAMMATION. Scav-
enger cells (
MACROPHAGES), summoned to the dam-
aged area release substances that destroy cell debris
and can damage surrounding healthy tissue. In
addition,
FREE RADICALS (extremely reactive oxi-
dants) cause chronic inflammation when produced
at joints.
ANTIOXIDANTS such as vitamin E, VITAMIN
C

, BETA-CAROTENE
, and related carotenoids and
FLAVONOIDS can quash free radicals and reduce
inflammation. Flavonoids are natural antioxidants
found in the pulp of citrus fruit, most vegetables
and fruits. High levels of fish and fish oil and seed
oils from flax, borage, and black currant lessen pain
and may help arthritic patients. These oils belong to
the omega-3 class of fatty acids, known to blunt
inflammation. They give rise to a family of
PROSTAGLANDINS (PG
3
) fat-derived hormones that
control inflammation.
Food allergy and food sensitivity can aggravate
inflammation in degenerative joint disease. A diet
that eliminates food allergens may minimize over-
reaction of the immune system in food-sensitive
people. Niacinamide has been used to improve the
range of joint motion and to help lessens pain and
swelling. Some studies have shown that
CHON-
DROITIN (a complex CARBOHYDRATE), when taken
with the amino sugar
GLUCOSAMINE, can signifi-
cantly relieve symptoms of osteoarthritis. In the
body chondroitin acts like a magnet, drawing
nutrient-filled fluids into tendons, ligaments, and
cartilage. This helps make the cartilage more shock
absorbent.

As a dietary supplement chondroitin can reduce
joint pain and inflammation and may help main-
tain or repair cartilage. It is still unclear how this is
achieved. However, patients who have taken chon-
droitin supplements show increased levels of
hyaluronic acid, a primary component of the fluid
that lubricates joints. These benefits seem to
increase when chondroitin is taken in combination
with glucosamine, an amino sugar needed by the
body to form connective tissue. Patients suffering
from osteoarthritis who took chondroitin and glu-
cosamine supplements showed reduced pain and
improved joint mobility.
482 ossification
The long-term safety of these supplements has
not yet been determined. There are some indica-
tions that glucosamine can increase blood sugar
levels, so people with diabetes should avoid taking
supplements that mix chondroitin with glu-
cosamine unless done under a doctor’s supervision.
(See also
ESSENTIAL FATTY ACIDS; OSTEOPOROSIS;
RHEUMATOID ARTHRITIS.)
McAlindon, Timothy E. et al. “Glucosamine and Chon-
droitin for Treatment of Osteoarthritis: A Systematic
Quality Assessment and Meta-Analysis,” Journal of the
American Medical Association 283 (2000): 1,469–1,475.
osteomalacia (adult rickets) An adult bone dis-
ease caused by chronic
VITAMIN D deficiency or by a

deficiency of
CALCIUM or PHOSPHORUS. In osteomala-
cia, bones do not calcify properly; they become soft
and flexible, leading to a distortion of the pelvis,
spine, and rib cage. Symptoms include pain in these
regions and progressive weakness. When the diet
contains adequate calcium and phosphorus, osteo-
malacia can easily be prevented with extra
VITAMIN
D
during the winter months. Vitamin D is manufac-
tured in the skin when exposed to sunshine; it has
been commonly added to milk and milk products
since the 1940s. (See also
OSTEOPOROSIS.)
osteoporosis A chronic degenerative disease due
to the loss of bone mass or increased bone porosity.
The term osteoporosis means, literally, porous bones.
The affected bones are deficient in
CALCIUM, phos-
phorus, and other minerals, and they contain less
structural protein. In contrast, another bone dis-
ease,
OSTEOMALACIA, results from soft bones due to
altered mineral ratios. Osteoporosis is the most
common bone disorder in America. It occurs much
more frequently in women than in men. Men have
larger bones, eat more calcium and get more exer-
cise than women, although alcoholic men are an
exception. Mineral loss from bones typically begins

in the 20s, and 50 percent of the bone loss in
women occurs before menopause. Postmenopausal
osteoporosis (type I) is the most common form; type
II osteoporosis occurs with
AGING. In both men and
women, symptoms include curved spine, loss of
height, and brittle, accident-prone bones, particu-
larly the spin and hip. Calcium is preferentially lost
from the long bones of the legs, the spine, the jaw
bone, the wrists and the ankles when there is not
enough calcium in the diet, or when it is poorly
absorbed. Loss of bone of the spine can lead to com-
pression fractures and a loss in weight frequently
associated with aging. With reduced bone support,
gums may be damaged and teeth may be lost.
The social and economic impact of osteoporosis
is enormous. An estimated 10 million Americans
have this disease, and another 34 million people
are estimated to have low bone mass, placing them
at increased risk for osteoporosis. About 1.5 million
fractures due to weakened bones occur each year
in the United States. With osteoporosis, fractured
bones mend slowly.
Most fractures associated with this disease occur
in the spine, hips, wrists, and ribs. The risk that
a woman will suffer a hip fracture during her
lifetime is the same as her combined risk for devel-
oping breast, uterine, and ovarian cancer. Half of
all women and a third of all men will suffer
an osteoporosis-related fracture after their 50th

birthday.
Hip fractures can be especially debilitating and
even deadly. One-fourth of patients who could
walk before a hip fracture are unable to do so once
the fracture heals. About a quarter of those who
suffer hip fractures after the age of 50 die within a
year after their injury.
The rate at which bone is lost also affects the risk
of osteoporosis. Contrary to common belief, bone is
a dynamic tissue; it is constantly being formed and
broken down. Until the early 20s, more bone is
made than broken down as growth progresses.
Bone mineral content of the spine and wrist
reaches a maximum density in the late 30s and
early 40s. After peak bone loss has been reached,
there is little change until the 40s, when the bal-
ance between synthesis and degradation shifts to
favor degradation. Bone loss accelerates at
menopause and continues at a high rate for about
10 years. Afterward, bone is lost at a rate of 0.2 per-
cent to 0.5 percent per year. Typically, a U.S. female
will lose between 30 percent and 50 percent of her
cortical bone (the spongy interior bone structure).
It has often been assumed that menopause triggers
bone loss. However, the rate of bone loss increases
rapidly between the ages of 40 and 44, much ear-
lier than menopause, which in the United States
occurs at an average age of 52.
osteoporosis 483
Osteoporosis is a complex disease involving both

genetic and environmental factors, including such
nonmodifiable factors as gender, ethnic back-
ground, body build, family history of osteoporosis,
and age. Nevertheless, osteoporosis is one of the
most preventable of the degenerative diseases.
Medical history affects the risk of osteoporosis as
follows:
• Hormone imbalance. Because hormones main-
tain bone structure, hormonal imbalances can
lead to osteoporosis. Examples include defi-
ciencies of estrogen due to surgical removal of
ovaries, and to postmenopause; Cushing’s syn-
drome (excessive production of
GLUCOCORTI-
COIDS by the adrenal glands); conditions that
lead to excessive glucocorticoids, as chronic
stress or overmedication with hydrocortisone;
and overproduction of hormones from the pitu-
itary gland; and cortisone and thyroid medica-
tions;
• Certain rare genetic diseases (Marfan’s syn-
drome, homocystinuria);
•
RHEUMATOID ARTHRITIS;
• Conditions that promote
ACIDOSIS, such as
chronic obstructive lung disease and possibly
diabetes;
• Milk sensitivity or milk allergy;
• Anorexia nervosa;

• Conditions that lead to severe calcium malab-
sorption. These include excessive use of medica-
tions, such as certain anticonvulsant drugs and
anticancer drugs that block calcium uptake; low
stomach acid production (hypochlorhydria,
achlorhydria); stomach surgery, and anti-ulcer
drugs, like cimetidine, which blocks stomach
acid production and limits calcium digestion).
Lifestyle factors play a major role in determining
the risk of osteoporosis, including:
• A lack of physical, weight-bearing exercise
(sedentary lifestyle, being bedridden). Exercise
such as walking, jogging, and dancing increases
bone density and delays bone loss at all ages. On
the other hand, strenuous exercise such as run-
ning a marathon can disrupt hormone balance
and increase bone loss.
• Excessive alcohol consumption contributes to
malnutrition and increased bone loss.
• Cigarette smoking increases bone degradation
and limits bone rebuilding.
• Stress, both emotional and physical—fear,
trauma, dehydration, surgery, and the like—can
lead to bone loss in many elderly persons,
depending upon the degree of calcium malab-
sorption, the absorbability of dietary calcium
and other lifestyle influences.
Various dietary factors affect bone strength and
bone turnover. These include a deficiency of cal-
cium, trace minerals, and vitamin D. High bone

density is a major factor in decreasing the risk of
bone loss, and strong bones require adequate
dietary calcium. Bones can be thought of as a bank
account: The larger the bone and the more calcium
it has, the more it can tolerate slow withdrawal as
the body ages. With age, the ability to absorb cal-
cium declines; this difference is made up by
increased production of hormones that promote
mineral loss from bone. Calcium deficiency is
linked to osteoporosis.
The
RECOMMENDED DIETARY ALLOWANCE (RDA)
for calcium in the United States is 800 mg for adult
women. The RDA for girls and young women
between the ages of 12 and 19 is 1,200 mg; they
generally get only 900 mg of calcium daily. Ameri-
can women generally consume less than 500 mg of
calcium daily after menopause, which increases the
risk of osteoporosis. The National Institutes of
Health recommends that postmenopausal women
not taking estrogen, and men over 65, consume
1,000 to 1,500 mg of calcium daily. The extra 1,000
mg they need to add could come from any one of
the following: supplementation with about 1,000
mg of calcium; consuming three cups of milk, two
cups of nonfat yogurt, four ounces of cheese, nine
ounces of sardines, or four to five cups of cooked
broccoli or kale daily. These portions of canned fish
and vegetables are much more of these foods than
most people want in a day. Furthermore, many

women decrease their intake of dairy products due
to milk sensitivity and lactose intolerance there-
fore, many may opt for calcium supplements.
MAGNESIUM is also quite important in maintain-
ing bone strength. Supplementation with magne-
484 osteoporosis
sium together with calcium may help prevent bone
thinning and actually help rebuild bone in post-
menopausal women with osteoporosis. A mild
magnesium deficiency increases the risk of osteo-
porosis. Magnesium deficiency is associated with
lowered levels of calcitriol, the active form of
VITA-
MIN D
(see below). Magnesium may help the secre-
tion of
PARATHYROID hormone, required for the
formation of adequate calcitriol.
In addition to major mineral nutrients, calcium,
and magnesium, many trace mineral nutrients
support calcium uptake and contribute to bone
strength.
BORON deprivation increases urinary
excretion of calcium, and adequate dietary boron
may cut the bone loss associated with menopause.
Boron may affect parathyroid hormone and the
activation of estrogen and vitamin D to calcitriol.
Adequate boron seems to diminish bone losses
associated with menopause.
COPPER plays a role in

calcium assimilation; it is required to stabilize
COL-
LAGEN, the structural proteins that help form the
matrix for calcification. Osteoporosis occurs with
copper deficiency; the bones of copper-deficient
animals are fragile. Fluoride was once thought to
be helpful in preventing osteoporosis, but a 1999
study by the Centers for Disease Control and Pre-
vention found no evidence to support that theory.
Vitamins
Vitamin D is required for calcium absorption. It is
converted to the hormone calcitriol, which stimu-
lates the production of calcium uptake proteins. Vit-
amin D is formed in the skin and is also obtained
from the diet, though milk and fortified cereals are
the only major sources. The liver and kidneys
process the vitamin to calcitriol. This activated form
of vitamin D is 10 times more effective in stimulat-
ing calcium absorption than vitamin D. Studies
show that elderly patients who remain indoors dur-
ing the winter without exposure to sunlight or its
equivalent run the risk of decreased calcium uptake.
VITAMIN C is required for normal collagen fiber
formation, and presumably for normal calcifica-
tion. Low
VITAMIN B
6
, FOLIC ACID, and VITAMIN B
12
deficiencies may contribute to the risk of osteo-

porosis. These vitamins play a role in the metabo-
lism of sulfur-containing
AMINO ACIDS, METHIONINE,
and
CYSTEINE. The accumulation of a by-product of
methionine degradation,
HOMOCYSTEINE, may occur
with deficiencies, and this buildup is implicated in
osteoporosis as well as other degenerative diseases.
VITAMIN K
plays a role in the formation of a cal-
cium-binding protein, osteocalcin. Proper mineral-
ization requires adequate levels of this protein.
Vitamin K is abundant in green leafy
VEGETABLES,a
possible factor in the protection against osteoporo-
sis afforded by a vegetarian diet.
Other dietary factors increase the risk of osteo-
porosis. Crash dieting or severe caloric restriction
leads to mineral malnutrition, including calcium
deficiency. Close examination of the typical Amer-
ican diet reveals a high protein intake but frequent
deficiencies of trace minerals required for bone
building. Urinary calcium losses appear to increase
with high-protein diets, irrespective of dietary cal-
cium. High-protein diets are also high-phosphate
diets, and excessive phosphate also increases cal-
cium excretion.
Vegetarian diets correlate with decreased preva-
lence of osteoporosis, although initial bone mass of

vegetarians may be equivalent to that of meat
eaters. Vegetarian diets provide less protein and
phosphorus but more boron. Each of the following
factors increases bone loss.
• Excessive sugar consumption increases calcium
excretion.
• Excessive coffee and caffeine intake appear to
increase calcium excretion. Generally, the more
coffee that is consumed, the less milk. Women
who drink milk throughout their adult lives
may be able to counter the bone-thinning
effects of coffee.
• Excessive soft drinks containing phosphate. A
high phosphate diet with limited calcium limits
calcium absorption and increases bone degrada-
tion.
• Excessive sodium has been linked to increased
risk of osteoporosis and increased urinary losses
of calcium.
• Decreased estrogen production after menopause
increases bone loss. Theoretically, estrogen stim-
ulates vitamin D to increase calcium intake; it
slows calcium loss by the kidneys; and it
increases production of a hormone to store cal-
cium in bone. With estrogen deficiency, osteo-
osteoporosis 485
clasts, cells that break down bone, are more sen-
sitive to parathyroid hormone, causing increased
bone breakdown. While estrogen therapy for
elderly women stops further bone loss and

decreases the risk of fractures of thinned bones
after menopause, alone it may not prevent
osteoporosis.
Recommendations
Patients should:
• consume enough calcium and magnesium. Girls
and young women can take calcium supple-
ments and eat calcium-rich foods to build up
their bone density during their growth years. A
daily consumption of up to 1,000 mg of calcium
before menopause and 1,500 mg daily after
menopause is recommended. People who are
susceptible to kidney stones need to consult
their physician before calcium supplementation.
Several hundred mg of magnesium are generally
well tolerated; more can lead to diarrhea.
• obtain enough vitamin D from fortified milk and
milk products to deposit calcium into bones.
Adequate sunshine enables the skin to make vit-
amin D.
• obtain enough manganese, copper, and zinc.
These minerals help with calcium utilization for
bone building.
• avoid excessive fiber supplements, high-protein
diets, and soft drinks with phosphate.
• stop smoking.
• exercise regularly throughout life. Walking
daily, cycling, dancing, bike riding, and similar
exercises are most beneficial in retaining cal-
cium in bone.

• avoid excessive amounts of antacids that contain
aluminum. Aluminum can interfere with nor-
mal calcium absorption and assimilation.
• consult a specialist regarding estrogen replace-
ment therapy after menopause. For calcium to
reverse osteoporosis after menopause, a woman
may need to take low doses of estrogen and to
exercise daily in addition to calcium supplemen-
tation. Who should not take estrogen? Women
who are obese, who have a history of breast
cancer or blood clotting problems. Estrogen
therapy requires medical supervision because of
potential side effects. (See also
OSTEOARTHRITIS.)
Marchigiano, G. “Calcium Intake in Midlife Women: One
step in Preventing Osteoporosis.” Orthopaedic Nursing
(September/October 1999): 11–20.
ovalbumin The major egg PROTEIN. Ovalbumin
represents about 25 percent of the total protein of
EGG white.
Overeaters Anonymous
(OA) An organization
that provides support groups based on the Twelve
Step Program of Alcoholics Anonymous. These
groups can help people deal with issues surround-
ing compulsive eating, bingeing and purging. There
are no dues, and participation is voluntary. It is run
entirely by volunteers.
Members of OA focus on getting control of their
own lives and identifying underlying emotional

issues, not on
DIETING, nor on losing weight, nor
even on food. There are no weigh-ins and no guar-
antees of weight loss. Eating disorder programs
managed by hospitals and clinics often send their
participants to OA to strengthen their own behav-
ior modification strategies. (See also
OBESITY;
WEIGHT MANAGEMENT.)
overweight In 1998 the federal government
adopted new standards for determining whether a
person is overweight or obese. Before then people
were considered overweight if their weight was at
least 10 percent to 20 percent over optimal body
weight. Obesity was defined as being more than 25
percent over the optimal body weight for men and
30 percent over the optimal body weight for
women.
Under the new standards a person with a
BODY
MASS INDEX
(BMI) of 25 or more is considered over-
weight. The BMI is determined by dividing a per-
son’s weight in kilograms by the square of his or
her height in meters. A healthy BMI falls between
19 and 25. A person with a BMI of 30 or above is
considered obese. (See also
DIETING; FAT; IDEAL BODY
WEIGHT
; WEIGHT MANAGEMENT.)

ovo-vegetarian One who eats plant-derived
foods and eggs. A lacto-ovo-vegetarian is one who
eats plant-derived foods, milk products, and eggs.
(See also
VEGETARIAN.)
486 ovalbumin
oxalic acid/oxalate An acid found in a variety of
vegetables that binds
CALCIUM very tightly. Oxalic
acid forms salts called oxalates with minerals, mak-
ing them less available for absorption.
SPINACH, beet
greens,
CHIVES, RHUBARB, and PARSLEY contain sig-
nificant amounts of calcium, but they also contain
high levels of oxalic acid. However, oxalic acid does
not block calcium uptake of
IRON or of the calcium
in other foods. It is not clear whether cooking
greens makes calcium more available. Even with
oxalates, these green leafy vegetables will supply
significant
TRACE MINERALS, plus VITAMINS and
FIBER
, and should be part of a BALANCED DIET.
Oxalic acid may be a potential by-product of vit-
amin C consumption in excess of amounts achiev-
able from dietary sources in cases of kidney disease
and of those prone to the formation of calcium
oxalate

KIDNEY STONES, based on anecdotal reports
in a small number of cases.
Oxalic acid consumption may be a problem for
people who are prone to kidney stones, or those
who eat a lot of
BRAN for fiber and whose diets are
high in oxalates and low in calcium.
MAGNESIUM
increases the solubility of calcium oxalate and
decreases the probability of kidney stones, and
VITA-
MIN B
6
reduces oxalate production. Getting enough
VITAMIN K is also important: Vitamin K assists in the
formation of a urinary protein that inhibits calcium
oxalate precipitation and helps inhibit kidney stone
formation. (See also
MALABSORPTION.)
oxaloacetic acid An acid that is both the starting
point and final product of the
KREB’S CYCLE. This
cycle plays a central role in the oxidation of
FAT, CAR-
BOHYDRATES, and AMINO ACIDS for energy production
by the body. Oxaloacetic acid receives incoming car-
bon atoms to form
CITRIC ACID. Sequential oxidation
steps release these carbon atoms as
CARBON DIOXIDE,

the ultimate end product, while regenerating
oxaloacetic acid. Oxaloacetic acid serves a second
role: It can accept nitrogen to generate the acidic
AMINO ACID, ASPARTIC ACID. It is also required to syn-
thesize
GLUCOSE (BLOOD SUGAR) from amino acids to
fuel the brain during
STARVATION. (See also CARBOHY-
DRATE METABOLISM; GLUCONEOGENESIS.)
oxidation The primary chemical reaction by
which chemical
ENERGY is released from food for
use by cells. The oxidation of fuel molecules in
foods involves the addition of oxygen atoms to car-
bon atoms and the removal of hydrogen atoms.
The ultimate oxidation product of carbon com-
pounds is
CARBON DIOXIDE. Indeed, carbon dioxide
in expired air comes from the direct oxidation of
FAT
, CARBOHYDRATE, PROTEIN, and other fuel mole-
cules by cells in the body.
Most oxidation takes place in small particles in
the cytoplasm known as mitochondria. These cel-
lular powerhouses consume more than 90 percent
of the oxygen that the cells use. They oxidize most
of the fuels to carbon dioxide, while producing
ATP.
This form of chemical energy is readily used to
power energy-requiring operations of the cell. The

total energy released by oxidations occurring in
cells is the same as when substances are burned in
a test tube. The difference lies in the fact that
within cells oxidation proceeds in small steps,
speeded up by
ENZYMES, in order to capture chemi-
cal energy efficiently. About 40 percent of the
potential energy trapped in the simple sugar
GLU-
COSE, for example, is captured as ATP.
Cellular oxidations require electron carriers
called
COENZYMES as enzyme helpers. The most
important are
NICOTINAMIDE ADENINE DINUCLEOTIDE
(NAD), derived from the B vitamin NIACIN, and
FLAVIN ADENINE DINUCLEOTIDE
(FAD), derived from
the B vitamin
RIBOFLAVIN
. In this process oxygen is
reduced to water (
METABOLIC WATER), also pro-
duced by mitochondria, which generate about 200
ml daily.
Many degradative enzymes function together as
METABOLIC PATHWAYS. Important energy-yielding
pathways oxidize glucose (
GLYCOLYSIS) and carbo-
hydrate, fatty acids and amino acids (

KREB’S CYCLE).
Most ATP formation occurs in mitochondria via a
pathway called
OXIDATIVE PHOSPHORYLATION.(See
also
AMINO ACID METABOLISM; CARBOHYDRATE META-
BOLISM; FAT METABOLISM.)
oxidative phosphorylation The oxygen-depen-
dent process of trapping chemical
ENERGY released
by the
OXIDATION of fuel molecules. Oxidative phos-
phorylation occurs in
MITOCHONDRIA, small particles
in cells that function as powerhouses. Cellular oxi-
dations in mitochondria release electrons that are
transported to oxygen. Their passage to oxygen is
oxidative phosphorylation 487
performed by a sequence of electron carriers and
enzymes known collectively as the
ELECTRON TRANS-
PORT CHAIN. When electrons are transported from
one electron carrier to the next and ultimately to
oxygen, a portion of the released energy is trapped
as ATP; the remainder is lost as heat. ATP is a chem-
ical form of energy universally used by cells to drive
energy-requiring processes, from the contraction of
muscle fibers and the transport of nutrients into
cells to the biosynthesis of cellular constituents for
cell growth and maintenance. Only mitochondria

possess the enzyme machinery for coupling the
flow of electrons to the reduction of oxygen to
water, and simultaneously to synthesize ATP.
Electron transport and ATP production can be
uncoupled, that is, oxidations can occur with
decreased ATP production. Various chemicals alter
the structure of mitochondria and act as uncou-
plers; certain environmental pollutants, poisons,
and drugs can interfere with ATP production, with
potentially disastrous effects on cellular metabo-
lism. Poisons like cyanide block electron transport,
hence ATP production, in cells. The drug dinitro-
phenol was once marketed as a weight loss aid
because it allowed more fuel to be burned with less
ATP production. But the use of dinitrophenol led to
excessive heat production, and it was banned.
Even large amounts of normal products such as
BILE PIGMENT, bilirubin, and fatty acids can act as
uncouplers. Certain patches of body fat called
brown fat possess mitochondria that can be hor-
monally uncoupled to produce heat to protect
newborn mammals, including infants. Thyroid
hormone and the nervous system can regulate the
efficiency of ATP production to a limited extent.
oxygen The element that accounts for approxi-
mately 21 percent of Earth’s atmosphere and is
essential for aerobic organisms. Animals require
ample oxygen to oxidize food to
ENERGY. Carbon
atoms are oxidized to

CARBON DIOXIDE, the first
metabolic waste product. Oxygen acts as the ulti-
mate oxidizing agent of fuel molecules, and it is
reduced to
WATER, the second waste product.
Oxygen taken up from air in the lungs must be
distributed throughout the body to all cells via the
circulatory system. Thus, oxygen is absorbed into
the bloodstream at the lungs, where it binds to the
oxygen carrier protein in
RED BLOOD CELLS called
HEMOGLOBIN. Oxygenated red blood cells are
pumped to tissues and oxygen is released in capil-
laries in response to acidic waste products and car-
bon dioxide from cellular metabolism, and to a low
oxygen concentration. Oxygen molecules simply
diffuse (migrate) into cells to participate in cellular
oxidations.
Oxygen can be partially reduced by enzymes to
form highly reactive molecules. Thus, activated
phagocytic cells (neutrophils, macrophages) pro-
duce the
FREE RADICAL superoxide, which can
destroy invading microorganisms. Overproduction
of superoxide during chronic
INFLAMMATION can
readily damage cellular components like proteins,
lipids, and
DNA. Cells possess defense mechanisms to
combat such agents.

COPPER, MANGANESE, and ZINC
activate the enzyme SUPEROXIDE DISMUTASE, which
neutralizes superoxide. (See also
ANTIOXIDANT.)
oxygen debt The amount of OXYGEN required to
support the physiologic response to strenuous
physical activity. Oxygen debt is characterized by
rapid or labored breathing (hyperventilation) and
increased metabolic rate that continues when
EXERCISE
ceases. During mild physical exercise,
oxygen delivered by the bloodstream is adequate
for muscles to oxidize
GLUCOSE (BLOOD SUGAR) com-
pletely to
CARBON DIOXIDE. The liberated energy
powers muscle contraction. However, during vigor-
ous exercise, oxygen delivery to muscle cells
becomes too slow to produce enough
ATP from the
oxidation of glucose and fatty acids to meet the
increased demand of muscle contraction. In this
case, additional ATP can be generated by the
incomplete oxidation of glucose through a process
called anaerobic
GLYCOLYSIS.
Glycolysis is the initial stage of carbohydrate
oxidation, which oxidizes glucose to a fragment
called
PYRUVIC ACID and produces ATP without the

participation of oxygen. In muscle cells, the
increased need for ATP outstrips the cells’ ability to
oxidize pyruvic acid during strenuous exercise. In
this case pyruvic acid is converted to
LACTIC ACID,
which diffuses into the bloodstream to be processed
to glucose by the liver. Panting at the end of stren-
uous exercise provides additional oxygen, which is
used to replenish cellular ATP and to rebuild
GLYCO-
488 oxygen
GEN (stored glucose) in muscle fibers. Lactic acid
accumulation may be partially responsible for the
fatigue and stress that accompany strenuous exer-
cise. During the recovery period, the oxygen debt is
repaid, lactic acid buildup is disposed of, energy
stores are replenished, and the breathing rate nor-
malizes. (See also
ANAEROBIC; CARBOHYDRATE
METABOLISM
.)
oyster
(Ostrea spp.) A saltwater shellfish belong-
ing to the family of bivalve mollusks. Although
indigenous to many parts of the world, oysters are
now farmed to avoid depletion and to minimize
their contamination from polluted water. East
Coast and West Coast varieties are available in the
United States. In oyster cultivation, small seed oys-
ters are first attached to a stationary support. As

they grow in size they are transferred to beds,
where their growth can be supervised. Tradition-
ally it was recommended that oysters and clams be
harvested only in months containing an “r” (Sep-
tember through April) to avoid contamination by
blooms of “red tide” microorganisms. These organ-
isms produce a toxin that accumulates in oysters
and mussels and can cause food poisoning. State
health departments monitor shellfish and may
restrict harvest in other months. A marine bac-
terium, Vibrio vulnificus, can infect warm, brackish
waters and infest shellfish such as oysters. The bac-
terium can cause blood poisoning in individuals
with a weakened immune system.
Fresh oysters are traditionally eaten raw with
lemon juice or sauce. However, the consumption of
raw or partially and cooked shellfish substantially
increases the risk of food poisoning and of diseases
transmitted by sewage, such as hepatitis A and
Norwalk virus. Cooked oysters are far safer. They
can be poached, browned, cooked on skewers, or
used in soups and sauces. Oysters canned in oil
contain more calories than fresh oysters. Oysters
are an excellent source of
ZINC, though different
varieties contain differing amounts. One oyster,
cooked (100 g), provides 90 calories; protein, 5 g;
carbohydrate, 5 g; fat, 5 g; cholesterol, 35 mg; cal-
cium, 49 mg; iron, 3 mg; zinc, 9 mg; thiamin, 0.15
mg; riboflavin, 0.29 mg; niacin, 2.1 mg.

oyster shell A common CALCIUM supplement that
is not a recommended calcium source because it
contains variable amounts of
LEAD, a widespread
environmental pollutant. Lead resembles calcium
and is incorporated into the bone and shells of
many organisms. (See also
HEAVY METALS;
SEAFOOD.)
oyster shell 489