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Cashew and Veggie Omelette (Serves 1)
1 teaspoon extra-virgin olive oil „2 cup (loosely packed) baby
spinach leaves
1 pat of butter
1 tablespoon cream cheese (organic
1 scallion, diced
„4 red bell pepper, diced
2 eggs, beaten
1 tablespoon dry-roasted unsalted
cashew pieces

In a 10-inch skillet heat the olive oil and butter over medium heat and
then add the scallion, red bell pepper, and cashew pieces and saut©.
When the scallion and pepper are soft, add the spinach and cream
cheese and stir-fry until the spinach wilts and the cream cheese starts to
melt. Transfer the saut©ed vegetables temporarily to a small plate. Pour
the beaten eggs into the skillet and allow them to cook until set, 1 to 2
minutes. Flip the omelette and then place the saut©ed vegetables on
one half and fold the omelette over them. Quantities can be doubled
for two people.
R E C I P E S , M E N U P L A N S , A N D G U I D E L I N E S F O R E AT I N G O U T

Avocado and Chicken Omelette (Serves 1)
1 teaspoon extra-virgin olive oil 2 tablespoons cooked and diced
chicken pieces
1 pat of butter
„2 small avocado, mashed
2 eggs, beaten

In a 10-inch skillet, heat the olive oil and butter over medium heat.
Pour in the beaten eggs and allow them to cook until set, about 2
minutes. Flip the omelette and then place the chicken and avocado on
one half and fold the omelette over. Quantities can be doubled for two

Breakfast Egg and Veggie Stir-Fry (Serves 1 for 3 breakfasts)
1 tablespoon extra-virgin olive oil or 6 tablespoons cooked brown rice
1 very small pat of butter Spice Hunter Deliciously Dill spice
3 scallions, diced mix, to taste*
„2 red bell pepper, diced 4“5 ounces fresh spinach, stems
removed (bagged spinach is ideal)
3 shiitake mushrooms (or other
variety), diced 6 eggs, beaten
4 tablespoons diced leftover chicken 2“3 tablespoons shredded Romano
or turkey, or deli turkey cheese
1“2 artichoke hearts, diced
Many people don™t have the time to prepare a protein-rich breakfast
before work. You can make this breakfast on a Sunday morning, eat a
third of it that morning, then place the other two servings in ramekins
(or small bowls), cover, and refrigerate. Microwave them for breakfast
on Monday and Tuesday morning.
Over medium heat, warm the olive oil in a nonstick wok and
saut© the scallions, pepper, and mushrooms until they soften. Then add
the turkey (or other meat), artichoke hearts, and brown rice, as
well as Deliciously Dill spice mix. Stir-fry the mixture, moving it
around with a spatula. Place the spinach leaves on top and allow them
to soften a little before stirring the ingredients together. Add the
beaten eggs and continue to stir-fry. When the eggs are just about
cooked (not runny), sprinkle on the Romano cheese and let it melt.
Divide the dish into three portions, placing one on your breakfast
plate and two into ramekins or other small bowls to save for later.
Serve with your choice of nonstarchy fresh fruit (for example, berries,
kiwifruit, cantaloupe) on the side.
134 F E E D YO U R G E N E S R I G H T

To vary the dish, try these substitutions: precooked baby shrimp or
precooked diced pork instead of turkey; hearts of palm instead of
artichoke hearts; Terrapin Ridge Wasabi Squeeze Garnishing Sauce
instead of Deliciously Dill Spice Mix.
*Available at most natural food stores

Exotic Rice Pudding (Serves 4)
2 cups ¬ltered or distilled water 2“3 tablespoons honey, or to taste
1 cup black or purple rice fresh fruit, such as banana slices or
(e.g., Forbidden Rice brand†) raspberries, and whipped cream
for garnish
1 cup premium (not light) coconut
3“4 teaspoons vanilla extract, or to

Bring the water to a boil over high heat in a 2-quart saucepan. Add the
rice, cover, reduce the heat, and simmer for 25 to 30 minutes, until most
of the water is gone. While the rice is cooking, pour the coconut milk
into a mixing bowl and add 2 to 3 teaspoons of the vanilla extract and
1 to 3 tablespoons of the honey. Whisk until the honey dissolves. When
the rice is done cooking and has cooled, transfer 3 cups of it to a bowl.
(Save the extra rice for use as a side dish with dinner or lunch.) Add the
coconut milk mixture to the rice and stir gently with a spoon. Add a lit-
tle more vanilla and honey to taste. Chill the rice pudding to allow the
rice time to absorb the coconut milk. Serve it topped with fruit and/or
a small amount of real whipped cream.

†Lotus Foods™ Forbidden Rice has a unique, rich ¬‚avor. It is available from health
food or specialty food stores, or go to www.lotusfoods.com.

Greek Yogurt with Honey (Serves 2)
8 ounces Greek yogurt‡ 1“2 tablespoons honey

Divide the yogurt into two serving bowls. Drizzle on the honey and
‡Available at Trader Joe™s or other specialty food stores
R E C I P E S , M E N U P L A N S , A N D G U I D E L I N E S F O R E AT I N G O U T

Fresh Banana and Nut Butter (Serves 2)
1 ripe banana almond or peanut butter

Slice the banana into circles, each about 1„2 inch thick. Spread some of
the nut butter onto each slice and serve.

Sample Two-Week Meal Plan
This meal plan is intended more as an idea generator rather than as a
rigid diet plan for you to follow for two weeks. Most people do not have
the time to cook three meals daily and instead are likely to make exten-
sive use of leftovers. Whatever you choose to eat, however, it is impor-
tant that you follow the dietary guidelines discussed in chapter 7. An
asterisk (*) indicates that the recipe is included in this chapter.

Sunday (Day 1)
Breakfast Breakfast Egg and Veggie Stir-Fry*, fresh fruit, and black tea
Lunch Chicken Caesar salad without croutons
Dinner Chipotle Shrimp Fajitas*, small side salad, and sparkling water

Monday (Day 2)
Breakfast Breakfast Egg and Veggie Stir-Fry* (reheated), fresh fruit, and
herbal tea
Lunch Deli Turkey and Cheese Wrap*
Dinner Salmon ¬llet pan-fried in olive oil, with green beans amandine

Tuesday (Day 3)
Breakfast Breakfast Egg and Veggie Stir-Fry* (reheated) and fresh fruit
Lunch Tuna Salad* on a bed of lettuce
Dinner Roasted Chicken with Rosemary and Garlic*, Saut©ed Fennel,
Olives, and Raisins*, and steamed green beans

Wednesday (Day 4)
Breakfast Avocado and Chicken Omelette* and fresh fruit
Lunch Chef™s salad without croutons
Dinner Fillet of Sole with Almonds and Parsley*, saut©ed spinach and
pine nuts, and a small baked yam
136 F E E D YO U R G E N E S R I G H T

Thursday (Day 5)
Breakfast Scrambled egg and chicken wrap in a low-carb whole-wheat
Lunch Chicken and Egg Salad* on a bed of butter lettuce
Dinner Shrimp with Artichoke Hearts and Dijon Sauce*, Simple Baked
Asparagus*, and purple or brown rice

Friday (Day 6)
Breakfast Simple, Fast Mini-Omelette* and fresh fruit
Lunch Simple Turkey Burger* (minus the bun) and side salad
Dinner Simple Trout Amandine*, Mashed Sweet Potatoes*, and
steamed broccoli and cauli¬‚ower

Saturday (Day 7)
Breakfast Eggs Florentine and fresh fruit
Lunch Chicken kebab with salad
Dinner Scallops with Saffron Sauce*, Roasted Carrots and Shallots*,
and purple rice

Sunday (Day 8)
Breakfast Quiche Lorraine (minus the crust) and fresh fruit
Lunch Chicken breast (minus the bun) and steamed broccoli
Dinner Oriental-style stir-fry with ¬nely sliced pork and vegetables

Monday (Day 9)
Breakfast Spinach and cheese mini-omelette
Lunch Cobb salad
Dinner Pan-fried salmon in olive oil and green beans almandine

Tuesday (Day 10)
Breakfast Slices of turkey, ham, and cheese with a fruit salad
Lunch Beef kebab grilled with onions, cherry tomatoes, and bell
Dinner Baked turkey breast, steamed broccoli, and red rice
R E C I P E S , M E N U P L A N S , A N D G U I D E L I N E S F O R E AT I N G O U T

Wednesday (Day 11)
Breakfast Omelette with salmon pieces
Lunch Chicken salad on a bed of lettuce or spinach
Dinner Fillet of sole lightly breaded with rice ¬‚our, served on top of
wilted spinach, and brown rice

Thursday (Day 12)
Breakfast Scrambled eggs with Romano cheese, with fresh fruit on the side
Lunch Greek salad with gyro meat
Dinner Baked cornish hens, Rosemary Carrots*, and spinach saut©ed
with shiitake mushrooms

Friday (Day 13)
Breakfast Denver omelette and fresh fruit
Lunch Smoked salmon, diced onions, and capers, along with a small
tossed salad
Dinner Baked chicken, steamed cauli¬‚ower, and brown rice

Saturday (Day 14)
Breakfast Eggs with turkey sausage and fresh fruit on the side
Lunch Chicken, vegetable, and brown rice soup
Dinner Oriental-style stir-fry with shrimp and bay scallops and

Navigating Restaurant Menus
Just a few years ago, waiters and waitresses were often puzzled when
customers ordered burgers without buns or steamed vegetables instead
of french fries. Since then various low-carbohydrate diets have moved
from the fringe to the mainstream, and many restaurants now under-
stand and are eager to accommodate their diners™ dietary preferences.
Still, you will have better luck ordering foods made with high-quality,
nutrient-dense ingredients at some restaurants than at others.
Although some fast-food restaurants (such as McDonald™s, Burger
King, and Wendy™s) are making more salads and low-carb offerings
138 F E E D YO U R G E N E S R I G H T

available, the reality is that most of their pro¬ts come from fries and
soft drinks, which are among the least healthy foods. If you are trying to
adhere to a nutrient-dense diet, the smells and the temptations at fast-
food restaurants may be too much to resist. There are other pitfalls as
well.A healthy-looking salad may still come with a dressing high in par-
tially hydrogenated vegetable oils, soybean oil, or cottonseed oil. It is
often best simply to avoid these restaurants.
From a nutritional standpoint, national low-end chain restaurants
(such as Denny™s or Carrow™s) are not much better than fast-food
places. Nearly all the food served is manufactured before being deliv-
ered to the restaurants, and many contain various sugars, re¬ned car-
bohydrates, and unhealthy oils. Again, it may be best to bypass these
You will have better luck at many ethnic restaurants, particularly
Greek, Middle Eastern, Japanese, and some Italian places. Seafood and
upscale new American cuisine restaurants usually offer healthy meals
as well. But you must be a responsible consumer and ask questions
before ordering.
They key is to avoid starchy foods (such as pastas or potatoes),
deep-fried foods (such as french fries or falafel), or large amounts of
white rice. Greek, Middle Eastern, and Italian restaurants typically use
olive oil to cook with, and you will do best ordering chicken, ¬sh, meats,
and vegetables. If you are trying to lose weight, skip the breadbasket
(simply ask the waiter to take it away). In Japanese restaurants a bowl
of miso soup or a plate of sashimi (sliced raw fish) is an excellent
choice; the sashimi avoids the rice that typically comes with sushi. The
new American cuisine tends to be very inventive and typically uses
high-quality ingredients in preparing ¬sh, chicken, and other dishes,
though such restaurants can sometimes be expensive. A baked or rotis-
seried half-chicken is usually a tasty and moderately priced meal.

Nutrition Plans for Protecting
and Enhancing Your Genes

Stress, Genes, and Nutrition

Scientists have long debated whether people are products of nature or
nurture. But one does not have to be a scientist to recognize the obvi-
ous: your thoughts and emotions are shaped by both your initial genetic
hardwiring and the many subsequent events (dietary, social, and envi-
ronmental) that rewire your genes. Conversely, your emotions and
thoughts directly and indirectly in¬‚uence the activity of your genes,
affecting your risk of disease and overall life expectancy.
Today many researchers are exploring what Ernest Rossi, Ph.D.,
the author of The Psychobiology of Gene Expression, has termed “psy-
chosocial genomics.”This merging of genetics and behavior looks at the
details of how genes in¬‚uence behavior and how behavior switches
various genes on and off in the brain and other organs. Of particular
relevance are the profound health consequences of chronic stress, a
nearly pervasive feature of modern life. Stress triggers changes in hor-
mone levels, which in turn modify the activities of multiple genes in
cells throughout the body. The consequences of these genetic changes
include the accelerated aging of brain cells, an increased susceptibility
to depression and anxiety, and a greater long-term risk of stress-related
physical illnesses, including heart disease.
This chapter describes some of the tantalizing research on the
142 F E E D YO U R G E N E S R I G H T

interplay of genes and behavior, with an emphasis on the undesirable
biochemical and genetic consequences of chronic stress. Because
persistent stress is so harmful to health, this chapter also recommends
specific nutritional supplements that reduce stress, apparently by
increasing the activities of genes involved in neurotransmitter produc-
tion. Like good wholesome foods, positive attitudes, feelings, and
behavior patterns can help nourish healthy genes. On your own you can
read about or take classes on a variety of stress-reducing and stress-
managing lifestyle habits.

The Interplay of Genes and Behavior
Just a few years ago, scientists believed that people had a ¬nite number
of brain cells. They now understand that the brain is a dynamic, chang-
ing, and adapting organ. Experiences can increase or decrease the pro-
duction of new brain cells, trigger gene transcription in brain cells
leading to elevated neurotransmitter production, and reshape synapses
(connections between brain cells) that influence how the brain
processes information.

Genes That Increase the Risk of Depression
Some types of genetic polymorphisms (variations in the structure of
genes) can heighten the risk of developing prolonged depression. As
you recall from chapter 5, polymorphisms in the structure of the meth-
ylenetetrahydrofolate reductase (MTHFR) gene reduce utilization of
folic acid, leading to inef¬cient methylation, elevated levels of homo-
cysteine, and impaired DNA synthesis and repair. Remarkably, the
same genetic variant that increases the risk of birth defects, heart dis-
ease, and cancer also increases a person™s risk of depression.
In a study of almost 6,000 Norwegians, Dr. Ingvar Bjelland and col-
leagues from the University of Bergen found that middle-aged women
with high homocysteine levels (a sign of low folic acid levels) were twice
as likely to be depressed, compared with those who had normal homo-
cysteine levels. Bjelland determined that most of the women consumed
adequate amounts of dietary folic acid but that the genetic polymor-
phism reduced the cellular processing of the vitamin. Folic acid™s role in
methylation feeds into the production of neurotransmitters, brain-
communication molecules involved in thinking and moods. When folic
acid levels are low, or when the vitamin is not being ef¬ciently utilized,
neurotransmitter levels may decline. Conversely, considerable other

research has shown that folic acid supplements may reduce depression
as well as enhance the bene¬ts of antidepressant medications.
A separate study, conducted by a team of researchers from the
United States, England, and New Zealand, showed that polymorphisms
in a different gene also increased a person™s susceptibility to depres-
sion. Terrie E. Mof¬tt, Ph.D., a psychologist at King™s College, London,
and colleagues studied the serotonin-transporter gene in 847 subjects.
This gene programs the construction of a key protein involved in mov-
ing serotonin to where it is needed in brain cells. Two versions of the
gene exist, one that is longer and very ef¬cient in transporting sero-
tonin and one that is shorter and less ef¬cient.
Mof¬tt found that people with the longer, ef¬cient gene for trans-
porting serotonin were not likely to become depressed after experi-
encing stressful life events, such as the loss of a job or the death of a
family member. However, people with one copy (from one parent) or
two copies (from both parents) of the shorter, less ef¬cient form of the
gene were far more likely to experience depression. Thirty-three per-
cent of people with one copy of the short gene became depressed, and
43 percent of people with two copies of the short gene became
depressed after experiencing stressful life events.
Mof¬tt™s research is particularly interesting because nearly all phar-
maceutical treatments for depression, including Prozac and Zoloft, are
intended to enhance serotonin levels in brain cells. Similarly, many nat-
ural treatments for depression also focus on improved utilization of
serotonin. For example, the amino acids tryptophan and 5-hydroxy-
tryptophan (5-HTP) are the biochemical precursors to serotonin, and
considerable research supports their benefits in the treatment of
depression and anxiety. It is plausible that people with the short
serotonin-transporter gene are more likely to bene¬t from tryptophan
or 5-HTP supplements. These two natural substances may help “load”
the genes and biochemical pathways involved in serotonin synthesis
and transport, just as folic acid supplements improve the activity of a
sluggish MTHFR gene.

How Shelley Solved Her Blues
Shelley, age ¬fty, began having serious bouts of depression and over-
reacting to the usual stresses of running her business. A physician
prescribed an antidepressant drug, which resulted in her gaining
weight but did not completely resolve her depression and anxiety.
He prescribed a second antidepressant drug, but it didn™t help.
144 F E E D YO U R G E N E S R I G H T

When Shelley went to a nutritionally oriented physician, he
tested her urine for kryptopyrrole, a chemical that binds to and
excretes vitamin B6 and zinc, two nutrients that in¬‚uence mood.
Shelly tested positive for this genetic predisposition, and work-
related stresses increased her production of kryptopyrrole and
loss of vitamin B6 and zinc. The effect was comparable to a de¬-
ciency of both nutrients.
Her physician recommended a high-potency B-complex sup-
plement, containing 100 mg of the major B vitamins. He also sug-
gested that she take extra vitamin B6 and inositol (a B vitamin
helpful in depression and anxiety), as well as zinc supplements.
Within two weeks Shelley™s depression lifted, and she now
remains calm in the face of work pressures.
She has also had a number of “side bene¬ts,” including higher
energy levels, better concentration, greater self-con¬dence, and
more restful sleep. Because of her increased energy, Shelley has
started to cook more foods from scratch and is eating more ¬sh
and vegetables. She has also lost her sweet tooth, along with ten
pounds in two months. “I haven™t felt this good in years,” she says.

Behaviors That Modify Genes and Brain Structure
Prenatal in¬‚uences and early childhood development can have lasting
effects on a person™s long-term mental and physical health. But rather
than being strictly a behavioral consequence, as psychologists have gen-
erally believed, these experiences actually affect gene activity in brain
cells, the creation of new brain cells, and the hardwiring of a child™s
developing brain.
For example, several teams of researchers have shown that prena-
tal and infant stresses reduce DNA synthesis and the production of
new brain cells, leading to smaller brain sizes and more fearful behav-
ior later in life. At the University of Wisconsin, researchers exposed
pregnant rhesus monkeys, close biological relatives of humans, to reg-
ular stresses, such as loud and startling sounds. The monkeys™ offspring,
more than two years after birth, exhibited elevated levels of cortisol,
one of the body™s prime stress hormones, reduced formation of brain
cells in some regions of the brain, and smaller brains.
Similarly, animal studies by Michael J. Meaney, Ph.D., of McGill
University in Montreal have shown that normal maternal care, such as
a mother rodent™s licking and grooming her pups, bolstered the pups™
long-term resistance to stress and stress-induced illness. In contrast, the

absence of this behavior increased the pups™ stress and led to higher
levels of pituitary and adrenal hormones, particularly cortisol. These
stress-related hormonal changes initiated a cascade of permanent alter-
ations in DNA structure and stress responses, eventually increasing
susceptibility to stress-related diseases. Although similar controlled
studies would not be ethical with human subjects, observational studies
have found that a lack of regular contact between mother and child can
lead to aloof, fearful, and abnormal behavior in children.
A multitude of other factors also affect brain development and the
activities of genes in brain cells. For example, some researchers have
proposed that the hormone insulin has effects similar to those of testos-
terone in gene activity and the organization of the fetal brain. Like
testosterone, insulin stimulates the growth of various types of brain
cells as well as synapses, and elevated insulin levels may program brain
cells for increased appetite and body weight.
Alcoholic beverages, which in¬‚uence behavior, also modify gene
activity, according to research by R.Adron Harris, Ph.D., the director of
the Waggoner Center for Alcohol and Addiction Research at the Uni-
versity of Texas. Harris and his colleagues analyzed the activity of ten
thousand genes in two regions in the brains of alcoholics. They found
that alcohol altered the activity of 191 genes, particularly those
involved in judgment and decision making. Among the affected genes
were those that have a role in the production of myelin, which forms a
protective sheath around nerve cells. Damage to the myelin sheath,
which also occurs in multiple sclerosis, can literally short-circuit the
transmission of nerve and brain signals. Thus, alcohol consumption
appears to do far more than just temporarily impair judgment and
re¬‚exes. It actually changes the behavior of genes in the brain.
Even negative emotions and so-called sour moods can stimulate
the secretion of cortisol and adrenaline and reduce the production of
serotonin. Brooding about bad things that have happened to you in life,
being irritable, or harboring resentment and anger all help sustain a
stress-hormone response. In the long term, such bad moods can sup-
press normal DNA synthesis, reduce production of new brain cells, and
reshape brain-cell connections in undesirable ways, helping set the
stage for chronic depression or anxiety.
One of the unhealthiest clusters of emotional traits consists of a
combination of aggressiveness, mistrust, and anger”what psychologists
define as a “hostile personality.” People with hostile personalities
tend to experience an especially strong stress response, characterized by
146 F E E D YO U R G E N E S R I G H T

elevated cortisol levels, and they are seven times more likely to die at a
younger age. Like alcohol, the intensity of this behavior can suppress
genes involved in normal thinking processes and healthy emotional
expression. Increasing intake of the nutritional building blocks of neu-
rotransmitters often can help reset brain chemistry and promote calmer
behavior. (See “Nutrients That Reduce Stress” later in this chapter.)

Antidepressant Drugs Boost Gene Activity in the Brain
One of the recent surprises in psychosocial genomics has been a better
understanding of how antidepressant drugs act on the brain. For years
physicians thought that antidepressant drugs, such as Prozac, work pri-
marily by improving cellular regulation of the neurotransmitter sero-
tonin. But research increasingly points to another mode of action: that
at least some antidepressant drugs actually stimulate the synthesis of
new DNA, brain cells, and connections between brain cells, a process
called neurogenesis.
Prozac and other antidepressant drugs, as well as the herb St. John™s
wort, begin boosting serotonin levels almost immediately. By doing so,
they should rapidly relieve depression. However, these therapies typi-
cally take two to four weeks to have a noticeable effect, suggesting that
they work by another mechanism.
This delay in exerting an antidepressant effect has led some
researchers, such as Rene Hen, Ph.D., of the National Institute of
Mental Health, to investigate whether these drugs might actually work
by generating new brain cells and synapses between brain cells, a
process that takes several weeks. Hen and several teams of researchers
have shown that antidepressant drugs do in fact increase neurogenesis.
In experiments Hen has shown that antidepressant medications lead to
a 60 percent increase in a key chemical marker of neurogenesis.
This research indicates that changes in DNA synthesis (required
for new cells) or gene activity lie behind many, if not most, of the bio-
chemical changes that occur in the brain (and likely the body as a
whole). In a very real sense, nearly everything that happens in our bod-
ies ultimately takes place on a genetic level.

The Cascading Health Effects of Stress
The stress response is one of the oldest and most universal biological
reactions to danger. It is deeply ingrained in both people and other ani-
mals, because for tens of millions of years, survival depended on quick

re¬‚exes and reactions to dangerous situations, such as being chased by

Stress Response and Stress Hormones
Stressful experiences trigger the nearly instant release of adrenaline
and glucocorticoid hormones, such as cortisol, from the adrenal glands.
These hormones in turn almost instantly shut down genes and meta-
bolic activities involved in most long-term physiological processes, such
as digestion, growth, healing, and reproduction. At the same time,
increased genetic activity immediately shifts nearly all the body™s bio-
chemical resources to the heart and skeletal muscles for either ¬ghting
or running, the well-known ¬ght-or-¬‚ight stress response. In the wild,
animals experience this type of stress only occasionally and only for
brief periods”often less than a minute”such as when a deer is being
chased by a cougar. The deer™s body literally marshals all its resources
to run for its life. If the deer successfully escapes, its adrenaline and cor-
tisol levels quickly return to normal.
This stress response”the biological equivalent of going from zero
to sixty in a second or two”was designed only for brief reactions to
danger. When it is sustained for long periods, as it often is in modern
society, the health consequences can be disastrous. Stress hormones
affect virtually every organ in the body, leading to chronic in¬‚amma-
tion, slow healing, high blood pressure, reduced circulation, and coro-
nary artery disease. Stress accelerates the aging of cells, particularly
brain cells, it suppresses DNA synthesis, and it interferes with thinking
and memory. It sets the biochemical stage for depression, anxiety, and,
in a severe form, posttraumatic stress disorder.
When the brain is chronically exposed to stress hormones, genes
turn on and off in response to unfamiliar stimuli. These hormones, at
high levels for long periods of time, can even be neurotoxic, leading to
an inhibition of neurogenesis and to brain damage and brain shrinkage.
As but one example, cortisol interferes with the activity of “brain-
derived neurotrophic factor,” a chemical that promotes neurogenesis.
Memory problems can be one consequence of these undesirable
changes in the brain.

Stress and In¬‚ammation
Chronic stress can also set the stage for in¬‚ammatory diseases, con-
tributing to arthritis, obesity, diabetes, heart disease, and many other
diseases. By activating the sympathetic nervous system, stress triggers a
148 F E E D YO U R G E N E S R I G H T

cascade of hormonal and chemical changes that promote chronic
in¬‚ammation. Some of the hormonal changes lead to the increased
production of cytokines, cell-communication molecules that include
interleukin-6 and C-reactive protein. These cytokines signal immune
cells to release other inflammation-promoting compounds, such as
prostaglandin E2”one of the body™s most potent promoters of in¬‚am-
mation. Underlying all of these biochemical changes are fundamental
alterations in gene activity, because genes ultimately program the pro-
duction of these biochemicals.
As I explained in The In¬‚ammation Syndrome, chronic in¬‚amma-
tion is involved in virtually every degenerative disease, including obe-
sity, diabetes, and heart disease. Cortisol and other stress hormones
increase the deposition of fat, particularly around the belly. Abdominal
fat cells exacerbate the situation because they secrete large amounts of
interleukin-6 and C-reactive protein, which help maintain both low-
grade in¬‚ammation and the body™s stress response.

Protecting Yourself from Stress-Related
Brain Damage
Scientists have gained an excellent understanding of the health conse-
quences of chronic stress, and over the years many alternative and
complementary practitioners have recommended a variety of stress-
reducing activities, such as deep breathing, yoga, and meditation.
Recently, in The Psychobiology of Gene Expression: Neuroscience and
Neurogenesis in Hypnosis and the Healing Arts, Ernest Rossi, Ph.D.,
developed a conceptual framework for activities that not only reduce
stress but also promote the growth of new and healthy brain cells and
synapses between neurons. The underlying idea is this: if stress can lead
to deleterious changes in brain cells, such as the inhibition of neuroge-
nesis, positive and life-enriching activities should foster the growth of
new brain cells and new connections between brain cells.
It turns out that creative endeavors and other positive life experi-
ences can promote neurogenesis. Writing in a medical journal, Rossi
explained that three general types of activities have been shown to
promote normal gene expression, neurogenesis, and healing. These
experiences involve novelty, environmental enrichment, and exercise.
Novelty includes exposure to new and satisfying experiences, such as
travel in another country. Environmental enrichment includes creative
pursuits, such as learning how to draw or attending a musical concert.

Exercise is known to increase production of muscle cells and energy
levels, but it also boosts levels of neurotransmitters such as serotonin.
Amazingly, changes in gene activity and brain cells begin taking place
within ten minutes of starting an activity and can continue for hours.
There is a good chance you believe that the stresses in your life are
inevitable or unavoidable. However, it is usually possible to moderate
your reaction to speci¬c stresses and to relax. When you reduce the
stress”or your response to it”you lessen stress-induced hormonal
changes and subsequent damage to brain cells. But there is a catch: you
must be willing to make some changes in your habits and attitudes.

Nutrients That Reduce Stress
As you have already read, many nutrients are involved in the synthesis
and repair of DNA, processes essential for the manufacture of new
cells, including brain cells. Many of these same nutrients also serve as
the chemical building blocks of neurotransmitters or coenzymes
involved in neurotransmitter production.
Chronic stress places a greater demand on these nutrients and can
diminish their levels. One consequence is an inhibition of both DNA
synthesis and the production of new brain cells. Stress can also reduce
neurotransmitter production and set the stage for depression, anxiety,
or panic attacks. When chronic stress is combined with nutrient de¬-
ciencies because of poor eating habits, the risk of mood disorders can
increase sharply.
A healthy diet and certain nutritional supplements create a friendly
environment for normal neurotransmitter production, as well as the
production of new DNA and cells, in the brain. Nutritious foods and
supplements strengthen the biochemical underpinnings of the brain.
Eating Habits. When you eat too many sugars and re¬ned carbohy-
drates, or when you skip a meal, you can feel your blood sugar drop.
Low blood sugar impairs your concentration and judgment, leaves you
tired and fuzzy-headed, and sometimes makes you feel irritable. These
symptoms often vanish after you eat something and your blood sugar
Unfortunately, the typical American diet is rich in sugary foods and
re¬ned carbohydrates, which are rapidly digested and quickly boost
blood-sugar levels. But this sudden elevation in blood sugar triggers the
rapid secretion of insulin, a hormone that lowers blood-sugar levels.
The result is a roller-coaster effect, with the ups and downs (and
150 F E E D YO U R G E N E S R I G H T

low-blood-sugar symptoms) occurring within a couple of hours. In
addition, high-carbohydrate foods lower the levels of vitamin B1, which
is needed to break down carbohydrates for energy.
Large amounts of coffee and other caffeine-containing beverages
(such as colas) compound the problem, in large part because they also
contain various sugars. Even without sugar, caffeine-containing bever-
ages trigger the release of stored sugar (glycogen) from the liver, with
the effect being similar to that of having a soft drink and a doughnut. Is
it any wonder that people™s impatience and irritability have appeared
to increase along with the number of Starbucks and drive-through
One part of the solution is emphasizing a diet rich in protein and
nonstarchy, high-¬ber vegetables, as described in chapter 7. Both pro-
tein and ¬ber help stabilize blood-sugar and insulin levels, which will
then help even out mood swings. The protein provides at least two ben-
e¬ts: it has little effect on blood-sugar levels, and some of the amino
acids derived from it are used to construct neurotransmitters. Fiber
slows the absorption of carbohydrates, thus moderating the swings in
blood-sugar and insulin levels.
B Vitamins. Discussed in chapter 5, the B-complex family of vitamins
has long been known as the antistress nutrients. Some of the B vitamins
are involved in DNA-synthesis and -repair processes, necessary for the
production of new cells in the brain and throughout the body. Many of
the B vitamins, such as vitamin B6, are needed for the body™s produc-
tion of brain-calming neurotransmitters, such as serotonin, taurine, and
gamma-amino butyric acid (GABA).
David Benton, Ph.D., a professor at the University of Wales, found
that 50 mg of vitamin B1 daily helped otherwise healthy young adults
feel more “composed and energetic.” In a separate study, Benton found
that a daily high-potency multivitamin helped improve the moods of
young women. The bene¬ts seemed most related to vitamins B2 and B6
in the multivitamin supplement.
Similarly, prison studies conducted by Stephen J. Schoenthaler,
Ph.D., a sociology professor at California State University, have found
that a simple multivitamin supplement, or replacing candy with fruit,
reduces the incidence of violence among incarcerated teenagers and
adults. Schoenthaler believes that proper nutrition improves the con-
nections between brain cells.
If you tend to be depressed or edgy, take a high-potency B-complex
supplement that includes 25 to 50 mg of vitamin B1.

Inositol. When we™re stressed, it™s easy to become panicky and overre-
act to situations. Several clinical studies have found that inositol, a
nutrient related to B vitamins, can be of great bene¬t in panic attacks,
depression, and obsessive-compulsive disorder. In a study at Israel™s
Barzilai Medical Center, Dr. Jonathan Benjamin compared inositol to
an antidepressant drug in 21 patients who had frequent panic attacks.
After one month of taking 12 to 18 grams of inositol daily, patients had
signi¬cantly fewer panic attacks. They also had fewer side effects com-
pared with people taking the drug.
To achieve Benjamin™s 12 to 18 grams of inositol daily, you would
have to take at least that many tablets or capsules. Your best source for
such a product would be a compounding pharmacy, a drugstore that
makes custom preparations. However, you may gain comparable ben-
e¬ts by taking 2 to 5 grams of inositol daily in combination with a high-
potency B-complex supplement, available at any health food store.
Vitamin C. When your intake of vitamin C is low, a situation that affects
as much as 30 percent of Americans, you are more apt to feel fatigued
and irritable. Brain cells are rich in vitamin C, which help temper stress
reactions by modulating catecholamines (brain chemicals) and other
neurotransmitters. In a recent study, Dr. Stuart Brody of the University
of Trier in Germany found that vitamin C supplements (3,000 mg daily)
improved the overall mood of patients and led to more frequent and
satisfying sexual activity.
Vitamin C is crucial to health, and most people do not consume
enough of it. Take a minimum of 500 mg of supplemental vitamin C
daily. A more ideal dosage, divided up once or twice during the day,
would be 1,000 to 3,000 mg. Read the ¬ne print on the label carefully to
avoid products with added sugars (including lactose).
Theanine. Although found in green tea, which contains caffeine, thea-
nine has a powerful anticaffeine, brain-calming effect. In fact, theanine
(an amino acid) may account for the many health bene¬ts of tea, from
promoting relaxation to lowering the risk of heart disease and cancer.
Some research suggests that theanine might also lower blood pressure,
one consequence of stress.
Theanine supplements are available in health foods stores. Follow
label directions, because products vary. Another and more preferable
option is to simply drink one or two cups of green tea daily.
Gamma-Amino Butyric Acid (GABA). This amino acid also functions
as a neurotransmitter, and nutritionally oriented physicians often use
GABA to treat anxiety. A study by researchers at the University of
152 F E E D YO U R G E N E S R I G H T

Utah School of Medicine identi¬ed part of the mechanism. GABA
helps the brain ¬lter out distracting signals”background noise, so to
speak”that impair thinking. For use as a supplement, take 500 to 4,000
mg of GABA daily.
Tryptophan and 5-Hydroxy-Tryptophan (5-HTP). During the 1980s
tryptophan, an essential amino acid, became a popular natural tran-
quilizer, sleep aid, and remedy for depression. Then, after hundreds of
people were sickened by a single contaminated batch of tryptophan
(imported from Japan) in 1989, the Food and Drug Administration
overreacted and banned it as an over-the-counter supplement.
Today tryptophan supplements are available only by prescription
in the United States. Ironically, it is necessary for health, remarkably
safe, and legally must still be added to baby formulas. Nonprescription
tryptophan supplements have been replaced by 5-HTP, a closely
related compound that is a precursor to serotonin. Like tryptophan, 5-
HTP has brain-calming, antianxiety, and antidepressant bene¬ts”and
an exceptional record of safety. For use as a supplement, take 300 to 400
mg before bedtime.

In the next chapter, we will consider the genetic components of some
common physical diseases and behavioral disorders, as well as the spe-
ci¬c nutrients that enhance gene function in these conditions.

Nutritional Recommendations
for Speci¬c Diseases, A to Z

Up to this point, we have focused on describing what is largely a
generic, or widely applicable, nutrition and lifestyle plan for maintain-
ing optimal gene function. In this chapter we focus more speci¬cally on
the relationship between genes and individual diseases and conditions.
These diseases and conditions involve (1) inborn genetic mutations or
variations, (2) acquired genetic damage, or (3) a combination of both
From a practical standpoint, the dif¬culty often becomes de¬ning
(and diagnosing) what is and is not a disease. For example, osteoporo-
sis and cancer are obviously diseases. But is an inherited polymorphism
in the vitamin D receptor (VDR) that may increase the risk of osteo-
porosis or cancer a disease as well? The question is not an easy one to
answer. We all are born with genetic variations or acquire genetic dam-
age that increases our risk of disease. A VDR-gene polymorphism may
help identify risk, but it cannot foretell disease with absolute certainty.
The risk associated with a VDR-gene polymorphism can be easily off-
set by spending more time in the sun (prompting the body™s manufac-
ture of vitamin D) or by taking vitamin D supplements.
The de¬nition of what is and is not a disease is in transition, a situ-
ation that begs us to be cautious in equating a genetic predisposition
154 F E E D YO U R G E N E S R I G H T

with an actual disease. In an article in the journal Science, Dr. James G.
Wright, a professor of surgery at Toronto™s Hospital for Sick Children,
wrote that “disease is a ¬‚uid concept in¬‚uenced by societal and cultural
attitudes that change with time and in response to new scienti¬c and
medical discoveries.” A case in point: in many societies people who
experience visions and hallucinations have been considered prophets
or shamans, but in Western nations such people are often diagnosed as
In trying to rede¬ne the meaning of disease, Wright suggested that
a disease should consist of three elements: “a state that places individ-
uals at increased risk of adverse consequences.” This approach tempers
the desire to classify all genetic variations as diseases, particularly when
the risk of such diseases can be modi¬ed through dietary and lifestyle
changes. Instead it considers whether the genetic variations pose a risk
of disease.
We begin by discussing the aging process, which re¬‚ects accumu-
lated damage to genes and other cell structures. Whether aging is or is
not an actual disease remains arguable. However, aging does entail
widespread genetic damage, which increases the risk of chronic degen-
erative diseases, including Alzheimer™s disease, cardiovascular diseases,
and cancer.

What Happens
Aging is the most common genetic disorder, and it affects every living
creature. It re¬‚ects the overall deterioration of our DNA, genes, non-
genetic cell structures, and biochemical processes. Until about age
twenty-seven for most people, their gene-repair mechanisms, along
with normal growth processes, stay ahead of ongoing damage to genes.
After this time gene damage begins to outpace repair mechanisms, and
people begin a slow but accelerating decline toward senescence. Some
tissues, such as those that form your heart, brain, or skin, may age faster
than others.
Some speci¬c genes are associated with an increased risk of age-
related diseases, such as the APOE E4 gene in heart disease and the
BRCA1 and BRCA2 genes in breast cancer. Conversely, some genes,
such as the -1082 GG gene, are associated with increased longevity and
resistance to chronic in¬‚ammation. However, no single gene appears
to play a governing role in the aging process. Rather, aging re¬‚ects

widespread damage to large numbers of different genes, ultimately
leading to a total cessation of activity.

The Gene Connection
Although theories of aging differ, most point to accumulated damage
to DNA, which impairs the normal functioning of genes. The most
widely held theory of aging centers on the destructive molecules called
free radicals, which primarily leak out of energy-producing chemical
reactions in cells. These chemical reactions are necessary for life”they
break down blood sugar and fats for energy”and so life, ironically,
contains the seeds for age-related gene damage and death. Other free
radicals form as a result of detoxi¬cation activities, such as breaking
down air pollutants and pesticides, as well as of immune activity, such as
when white blood cells use free radicals to destroy infectious bacteria.
As people age and acquire genetic damage, their genes become less
stable and reliable, leading to incorrect genetic programming and
increased cellular malfunctioning. The two most common causes of
death in developed nations are heart disease and cancer, both of which
re¬‚ect gene-based defects in immune function and related biochem-
istry. Neither heart disease nor cancer”or any other age-related
degenerative disease, for that matter”results from the failure of a sin-
gle gene. Rather, age-related diseases develop from what could best be
described as a genetic “system failure” involving damage to dozens, and
often hundreds, of different genes.
The ¬rst target of free radicals is the nearest: mitochondrial DNA,
which largely programs energy production. As mitochondrial genes are
damaged, energy production becomes less ef¬cient, leading to the cre-
ation of still more free radicals. These free radicals react with and dam-
age proteins and fats in the cell, as well as with nuclear DNA, the
source of most of our genes.
At the same time, a multiplicity of other deleterious changes occur.
Consumption of excess calories, particularly starches and sugars,
increases both blood-glucose and insulin levels. Glucose, particularly
when elevated to prediabetic and diabetic levels, autooxidizes”that is,
begins a chain reaction that generates more free radicals. Meanwhile,
elevated levels of insulin promote the activity of a variety of genes
involved in inflammation and stress-hormone responses. This gene
activity may be increased further through injuries and infections and by
psychological stresses.
In¬‚ammation, while necessary to protect against infection and to
156 F E E D YO U R G E N E S R I G H T

initiate healing, may become systemic, particularly if the diet is low in
antioxidants and antiin¬‚ammatory fats (such as omega-3 ¬sh oils and
gamma-linolenic acid). In fact, low-grade in¬‚ammation is known to
increase with age, partly re¬‚ecting increased immune-cell activity to
dispose of aging, malfunctioning, and dead cells. Chronic psychological
stresses increase levels of the stress hormone cortisol, which in turn
elevates blood glucose and insulin and helps set the stage for abdomi-
nal obesity.

What You Can Do
With this age-related genetic deterioration comes a decline in our
assimilation and utilization of all nutrients. Because nutrients are the
most basic building blocks for each of the body™s other biochemicals,
the consequences of this growing inef¬ciency cascade can affect every
aspect of health. For example, levels of most hormones decline with
age, bone density cannot be maintained and decreases, the number of
muscle cells decreases, and the immune system™s ability to resist infec-
tion decreases.
Two steps can signi¬cantly slow the age-related accumulation of
free-radical damage. One is building up and maintaining, over many
years, a nutritional reserve that improves your body™s ability to resist
genetic and nongenetic cell damage. The other way is to “load” cells
with speci¬c nutrients, such as B vitamins and free-radical-neutralizing
antioxidants, to enhance DNA functioning and to reduce damage.
The nutritional-reserve concept is a long-term strategy for mini-
mizing DNA and cell damage. It is best applied as early as possible in
life, though it can provide striking benefits at any age. The dietary
guidelines in chapter 7 describe a nutrient-dense diet, emphasizing
quality protein and fresh nonstarchy vegetables, which supports this
nutritional reserve. Many studies have shown that variations of this
diet, such as the Mediterranean diet, reduce the risk of heart disease
and cancer. Following this type of diet can also help you look younger
as well as feel younger. In one recent study, researchers have reported
that people who ate diets rich in ¬sh, vegetables, and olive oil had fewer
skin wrinkles compared with people who consumed sugary soft drinks,
pastries, and potatoes.
Many studies have shown that nutritional supplements can effec-
tively load the body™s cells and reduce DNA, gene, and chromosome
damage. Nutrient loading is comparable to saturating gene-dependent
biochemical pathways in the body. This approach does work”human

studies routinely ¬nd that blood and tissue levels of nutrients increase
after supplementation, usually with improvements in clinical symptoms.
Genetic polymorphisms that increase the risk of disease are also
responsive to higher levels of nutrients. For example, supplemental folic
acid and vitamin D offset polymorphisms that reduce the metabolism of
these vitamins. By loading or saturating the genes™ biochemical path-
ways, inef¬cient genes are given the ability to function normally and
prevent disease. The effect of not maintaining high levels of vitamins
and minerals, through either diet or supplements, has the same net cel-
lular effect as radiation damage to DNA, according to the eminent cell
biologist Bruce N.Ames, Ph.D., of the University of California at Berke-
ley. That alone is a compelling reason to supplement. And although
many nutrients (except re¬ned starches and sugars) are essential for
health, those discussed in chapters 4, 5, and 6 are especially important.
It is difficult to design or recommend a single supplement that
will suit every lifestyle or health concern. For the sake of relative
simplicity, the following dietary supplement provides moderately high
levels of the nutrients needed to ensure normal functioning of your
genes and cells.

An “Ideal” Daily Supplement
If you want to maintain (or improve) your health with relatively few
pills and capsules, shop for a supplement that contains all or most of the
following vitamins and minerals, and strive for the dosage recommen-
dations. Although this formula does not represent a real product, you
should be able to ¬nd comparable multivitamin and multimineral sup-
plements. When shopping, ask for a high-potency multivitamin supple-
ment and a regular-potency mineral supplement. The vitamin-like
nutrients will likely have to be purchased as individual supplements.
vitamin A 5,000 IU
vitamin B1 10“50 mg
vitamin B2 10“50 mg
vitamin B3 10“75 mg
vitamin B6 10“75 mg
vitamin B12 75“500 mcg
biotin 75“200 mcg
158 F E E D YO U R G E N E S R I G H T

choline 50“100 mg
folic acid 400“800 mcg
inositol 50“100 mg
pantothenic acid 75“100 mg
vitamin C* 500“3,000 mg
vitamin D 400“800 IU
vitamin E 200“400 IU
vitamin K 50“100 mcg

calcium* 800“1,000 mg
chromium* 200“400 mcg
copper 2“4 mg
iodine 50“150 mcg
iron† 0“10 mg
manganese 5“10 mg
magnesium 200“400 mg
phosphorus ‡ 0 mg
potassium 10“50 mg
selenium 200 mcg
zinc 15“30 mg

coenzyme Q10* 30“100 mg
carnitine* 500“1,000 mg
alpha-lipoic acid* 50“100 mg
carotenoids 10“20 mg
¬‚avonoids 100“200 mg

*Individual supplements (rather than multiples) will likely be required
to achieve these dosages.

Men and postmenopausal women may not need supplemental iron.
People with hemochromatosis or other iron-storage disorders should
not take any supplemental iron.

Although phosphorus is an essential nutrient, it is not usually required
supplementally, because most foods (as a result of high-phosphorus
fertilizers) are typically rich in this mineral.

Alzheimer™s Disease
What Happens
Alzheimer™s disease is the most common type of dementia (senility)
and accounts for about two-thirds of all cases. An estimated 4 million
Americans currently have some degree of Alzheimer™s disease. The
Chicago-based Alzheimer™s Foundation predicts that more than 14 mil-
lion people will have the disease by the year 2050. While these numbers
may be in¬‚ated, the prevalence of Alzheimer™s disease is likely to grow
as the overall population ages.
Symptomatically, Alzheimer™s disease is characterized by a severe
deterioration in memory combined with a decline in at least one other
cognitive function, such as language skills, perceptions, or emotional
reactions. In later stages it leads to a loss of motor skills and independ-
ence in day-to-day activities, such as grooming and going to the bath-
room. Because an accurate diagnosis can be determined only by
autopsy, physicians use a variety of criteria to assess whether a senile
patient has “probable” Alzheimer™s disease.
On a biochemical level, Alzheimer™s disease is characterized by
clumps and tangles of beta-amyloid protein around brain cells. Beta-
amyloid protein interferes with normal brain-cell activity as well as
with the production of new brain cells.
Cerebrovascular disease is the second most common cause of
dementia. Ministrokes reduce blood flow to various regions of the
brain and increase localized production of harmful free radicals. Brain
injury from cerebrovascular disease sometimes overlaps with the beta-
amyloid deposits characteristic of Alzheimer™s disease.

The Gene Connection
Researchers have identi¬ed several genes that are strongly associated
with early-onset Alzheimer™s disease, which is relatively rare. These
genes are not usually present in the more common late-onset
Alzheimer™s disease.
However, the apolipoprotein E4 (APOE E4) gene has been con-
sistently associated with a higher risk of late-onset Alzheimer™s disease.
Apolipoprotein E is a constituent of low-density lipoprotein (LDL),
the blood™s carrier of vitamin E, vitamin A, and carotenoids. People
with the APOE E4 gene also have elevated cholesterol levels and a
higher risk of coronary heart disease. However, not every person with
this gene will develop Alzheimer™s disease, suggesting that other genes,
160 F E E D YO U R G E N E S R I G H T

dietary factors, and lifestyle habits in¬‚uence the risk of Alzheimer™s
Elevated levels of homocysteine are strongly associated with an
increased risk of Alzheimer™s disease. In fact, people with blood levels
of homocysteine above 14 micromoles per liter of blood are two to four
times more likely to develop Alzheimer™s disease, compared with those
who have normal homocysteine levels. In general, the elevated homo-
cysteine is related more to low intake of folic acid and other B vitamins
rather than to variations in the gene coding for methylenetetrahydro-
folate reductase. Abnormally high levels of homocysteine, a conse-
quence of low B-vitamin intake, is toxic to brain cells and also damages
blood vessels in the brain.
Growing evidence points to chronic low-grade cerebral in¬‚amma-
tion as a cause of Alzheimer™s disease. Such in¬‚ammation may be the
result of serious brain injuries earlier in life. During the in¬‚ammatory
reaction to injury, the body produces large numbers of free radicals,
which stimulate the formation of beta-amyloid protein in the brain.

What You Can Do
Several studies have found that high intake of vitamin E, in either
foods or supplements, can reduce the risk of developing Alzheimer™s
disease. The vitamin helps neutralize free radicals, has mild antiin¬‚am-
matory properties, and also protects brain cells from beta-amyloid
Martha Clare Morris, Sc.D., of the Rush“Presbyterian“St. Luke™s
Medical Center in Chicago found that high intake of vitamin E reduced
the risk of Alzheimer™s disease by 70 percent. However, people with the
APOE E4 gene, which increases the risk of Alzheimer™s disease, were
most likely to bene¬t from the vitamin. A more recent study by Peter
P. Zandi, Ph.D., of Johns Hopkins University found similar bene¬ts
among people who had taken vitamin E and C supplements.
In a Dutch study of 5,395 people, Dr. Marianne J. Engelhart of the
Erasmus Medical Center in Rotterdam reported that high dietary
intake of vitamin E reduced the risk of Alzheimer™s disease by 18 per-
cent overall. However, smokers who ate a lot of vitamin E“rich foods
reduced their risk of Alzheimer™s disease by 42 percent.
Very large dosages of vitamin E (2,000 IU daily) have also been
shown to slow the progression of late-stage Alzheimer™s disease,
according to a large clinical trial by Mary Sano, Ph.D., of the Columbia

University College of Physicians and Surgeons. Although the subjects™
cognitive functions did not improve, they were able to take care of
themselves (such as performing personal grooming) much longer com-
pared with patients taking a placebo. In a follow-up study, Sano is
trying to determine whether vitamin E supplements will slow the pro-
gression of Alzheimer™s disease in its early stages.

A serendipitous discovery by German physicians found that daily sup-
plements of alpha-lipoic acid (600 mg) might halt cognitive decline in
Alzheimer™s disease. The physicians used alpha-lipoic acid to treat dia-
betic complications in a patient also diagnosed with mild Alzheimer™s
disease. The patient™s cognitive functions stabilized after regular alpha-
lipoic acid supplementation. Dr. Klaus Hager and his colleagues used
alpha-lipoic acid to treat eight other mild-to-moderate Alzheimer™s
disease patients for one year. Using standard medical tests for assessing
the disease, Hager found that the patients™ cognitive functions remained
stable during this time. Normally their cognitive skills would have
declined appreciably.
Animal studies conducted at Oregon State University have found
that a combination of alpha-lipoic acid and acetyl-L-carnitine (a form
of carnitine) can improve memory and lead to a partial reversal of the
aging process. These two nutrients, described in chapter 4, reduce free-
radical damage to both DNA and RNA and increase energy activity in
brain cells.

Both nutrients lower blood levels of homocysteine and are involved in
the body™s production of new DNA and cells. Low levels of either folic
acid or vitamin B12 doubled the risk of developing Alzheimer™s disease,
according to research by Hui-Xin Wang, Ph.D., of the Karolinska Instu-
tute in Stockholm. Conversely, maintaining normal to high intake of
these nutrients, through diet or supplements, reduced the risk of
Alzheimer™s disease. In fact, some cases of dementia may be caused by
nothing more than a de¬ciency of vitamin B12, which is easily corrected
through supplementation.

This herbal remedy, long recommended for improving memory, has
been shown to increase the activity of ten key genes in the brain, in¬‚u-
encing memory, speech, logical thinking, and emotional responses. Its
162 F E E D YO U R G E N E S R I G H T

bene¬ts in slowing Alzheimer™s disease, while not always consistent, are
extremely promising. In a study using a proprietary extract of ginkgo,
Dr. Pierre L. LeBars of the New York Institute for Medical Research
found that the herb (EGb 761 extract, 40 mg three times daily) moder-
ately increased cognitive performance and social functioning in patients
suffering from dementia.

Birth Defects
What Happens
Birth defects result from signi¬cant alterations in DNA and genes dur-
ing the growth and development of a fetus. Pregnant women who con-
sume low levels of vitamins have an increased risk of delivering a child
with some types of birth defects. This section focuses on several com-
mon birth defects that can be prevented, or ameliorated after birth,
through improved diet and supplements.

A cleft lip, which is relatively common, is a split in the middle of the
upper lip, whereas a cleft palate is characterized by a hole in the roof of
the mouth. Together they are among the most common of all birth

In spina bi¬da, the neural tube, which develops into the brain and spine,
fails to close during the ¬rst month of gestation. Very mild cases may be
identi¬ed by only a tuft of hair at the bottom of the spine. In more
severe cases, the spinal cord is exposed at birth. Nerve damage, paraly-
sis of the lower body, and a lack of bladder control are common conse-
quences of spina bifida. Other types of neural-tube defects include
encephalocele, in which the brain protrudes through the skull, and
anencephaly, the complete absence of the brain and spinal column.

This common genetic disorder is characterized by the existence of a
third copy of the twenty-¬rst chromosome (and all of the genes nor-
mally found on that chromosome). It results in “mongoloid” physical
features, mental retardation, a greater risk of developing leukemia and
early-onset Alzheimer™s disease, and reduced life expectancy. Although
the underlying genetic disorder causing Down syndrome cannot be

changed, many of the associated biochemical problems can be circum-
vented through high-dose vitamin and mineral supplements and thy-
roid medications, leading to improved intelligence and appearance.

Although technically not a birth defect, the development of brain can-
cer early in life points to subtle, as-yet-unidenti¬ed prenatal defects or
damage to brain-cell DNA. At least nine studies have shown that preg-
nant women who eat large amounts of N-nitroso compounds, found in
hot dogs and many luncheon meats, have children with a substantially
higher risk of brain cancer.

The Gene Connection
Women who carry polymorphisms in the gene programming for meth-
ylenetetrahydrofolate reductase (MTHFR), and who do not consume
adequate amounts of folic acid (and other B vitamins), are more likely
to have children with cleft lip, cleft palate, and spina bi¬da. As you read
in chapter 5, folic acid and several other B vitamins play fundamental
roles in the production of DNA, needed for the creation of new cells.
During pregnancy a woman™s folic acid requirements increase substan-
tially to support the rapid growth of her fetus.

Regine P. M. Steegers-Theunissen, Ph.D., of University Medical Center
in the Netherlands recently compared the dietary habits of the mothers
of 179 women who delivered children with a cleft lip, a cleft palate, or
both conditions with mothers of 204 children without the birth defects.
Steegers-Theunissen reported in the Journal of Epidemiology that
women with polymorphisms in the MTHFR gene, who also consumed
low levels of dietary or supplemental folic acid, were six to seven times
more likely to deliver a child with cleft lip or palate.

In the 1960s researchers in Wales noted that women with low dietary
intake of folic acid were more likely to have children with spina bi¬da
and other neural-tube defects. It took until the late 1980s for medical
journals and professional medical societies to of¬cially recognize the
fundamental importance of folic acid in preventing spina bi¬da. More
recent research has shown, not surprisingly, that some MTHFR poly-
morphisms may increase the risk of spina bi¬da, most likely by reduc-
ing folic acid activity. In addition, animal studies have clearly shown
164 F E E D YO U R G E N E S R I G H T

that an elevated level of homocysteine (the result of low B-vitamin
levels) is by itself toxic to embryos, causing spina bifida and other
neural-tube defects. Today the March of Dimes, known for its antipolio
campaign of the 1950s, has become a leading advocate of folic acid sup-
plementation before and during pregnancy.

Although the role of poor maternal nutrition in the development of
Down syndrome has not been delineated, research on other types of birth
defects points to its being a critical factor. In addition, the risk of deliv-
ering an infant with Down syndrome increases with a woman™s age,
suggesting that age-related deterioration of a woman™s eggs (and the
DNA in those eggs) plays a role. In experiments researchers have
shown that the DNA of people with Down syndrome is more suscepti-
ble to free-radical damage and is not ef¬cient at repairing itself.

See page 166.

What You Can Do
Researchers from the Centers for Disease Control recently reported
that folic acid or a multivitamin supplement containing folic acid, taken
by a pregnant woman, reduces her risk of delivering a child with any
type of birth defect.

In her above-mentioned study, Steegers-Theunissen found that women
who consumed large amounts of folic acid from foods (such as leafy
green vegetables) or supplements had a relatively low risk of bearing
children with a cleft lip or a cleft palate. This lower risk was evident in
women with either MTHFR gene polymorphisms or a normal MTHFR
gene. In a separate study, Scottish and Brazilian researchers found that
women who took vitamin supplements had about a 40 percent lower
risk of delivering children with either a cleft lip or a cleft palate.
As a general rule, if you are of childbearing age, take a moderately
high-potency multivitamin supplement with 400 mcg of folic acid. If
you have already given birth to a child with a cleft lip or a cleft palate
and plan to become pregnant again, take a multivitamin supplement
and increase your total folic acid intake to 1,000 to 2,000 mcg day. If
you were born with a cleft lip or a cleft palate, ask your physician to

measure your homocysteine levels; the birth defect may increase your
B-vitamin requirements.

Researchers have clearly demonstrated that folic acid supplements
(400 to 800 mcg daily) or multivitamins containing folic acid can signif-
icantly reduce a woman™s risk of delivering an infant with spina bi¬da
or other neural-tube defects. The timing of supplementation is critical.
The neural tube forms and closes between the seventeenth and thirti-
eth days after conception (or four to six weeks after a woman™s last
menstrual period)”which is usually before many women realize they
are pregnant. Taking supplements after this time will not reduce the
risk of birth defects. For this reason the March of Dimes, the U.S. Pub-
lic Health Service (USPHS), and other organizations recommend that
all women of childbearing age take a daily multivitamin that contains
400 mcg of folic acid.
If you already have had a pregnancy affected by spina bi¬da (or
other neural-tube defect, the USPHS recommends that you take 400
mcg of folic acid daily if you are not planning to become pregnant.
However, if you have delivered an infant with spina bi¬da and you do
plan to become pregnant again, the USPHS recommends that you take
4,000 mcg of folic acid daily starting at least one month before trying to
become pregnant.
Lest we ignore the overall diet, a study published in the American
Journal of Clinical Nutrition reported that women who ate large
amounts of dietary sugars (such as sucrose and high-fructose corn
syrup), other highly re¬ned carbohydrates, and potatoes had a higher
risk of delivering infants with spina bifida and other neural-tube
defects. Such a diet is typically low in B vitamins, quality protein, and

In the 1950s Dr. Henry Turkel began developing a regimen for treating
some of the genetic consequences of Down syndrome. His program,
which grew out of his earlier work on genetics and biochemistry, con-
sisted of giving patients with Down syndrome moderately high levels of
vitamins and minerals, plus some prescription drugs (such as thyroid
medication). Turkel found that the combination of vitamins, minerals,
and medications could offset many of the disastrous consequences of
Down syndrome. While his nutrition-medication program cannot alter
166 F E E D YO U R G E N E S R I G H T

the genetic cause of Down syndrome, it did appear to improve overall
gene function and biochemistry.
Turkel found that the earlier a child began receiving supplements,
the more normal his or her intelligence and appearance would be by
the mid- to late teens. Although Turkel had been recognized for his role
in developing lifesaving medical equipment during World War II, his
work with Down syndrome was largely ignored by medical organiza-
tions. Many people have continued recommending nutritional pro-
grams similar to Turkel™s, including Bernard Rimland, Ph.D., the
director of the Autism Research Institute in San Diego ([619] 281-7165
or www.autism.com/ari/), and Kent MacLeod, B.Sc. Pharm., of Nutri-
Chem in Ottawa, Ontario ([613] 820-9065 or www.nutrichem.com).
Recent research on nutrition and Down syndrome appears consis-
tent with Turkel™s ¬ndings. Dr. Bruce A. Yankner of the Harvard Med-
ical School has reported that brain cells in children with Down
syndrome produce three to four times more free radicals, compared
with normal children. These free radicals likely exacerbate damage to
brain-cell DNA, interfere with cognitive development, and contribute
to the increased the risk of Alzheimer™s disease.
Yankner reported that antioxidants, including vitamin E and N-
acetylcysteine, could, in test tubes, prevent the destruction of brain cells
obtained from children with Down syndrome. Meanwhile, researchers
at the University of Chile have reported that vitamin E can reduce
chromosome damage in lymphocytes obtained from people with Down
syndrome. Subsequent research by Yankner indicated that impaired
mitochrondrial function was also involved in Down syndrome. That
¬nding suggests that supplemental alpha-lipoic acid, coenzyme Q10,
and carnitine might also be helpful. (See “Fatigue and Chronic Fatigue
Syndrome” later in this chapter.)

Dr. Susan Preston-Martin of the University of Southern California at
Los Angeles led a team of international researchers who investigated
the relationship between maternal use of multivitamins during preg-
nancy and the subsequent risk of brain cancer in children. Her study
focused on 1,051 children with brain cancer and 1,919 healthy children.
She found that pregnant women who took multivitamin supplements
were, overall, 40 percent less likely to have children who developed
brain cancer. However, women who took vitamins for the greatest
length of time had children with the lowest risk of brain cancer.

What Happens
All normal cells have clear biological functions and a cycle of life,
beginning when they are created. When cells malfunction or get old,
this life cycle ends with apoptosis, a type of biologically programmed
self-destruction. In contrast, cancer cells do not have a normal biologi-
cal function, and they do not have the built-in failsafe of apoptosis.
Cancer cells grow uncontrollably, destroying organs and draining the
body™s nutritional resources for energy, normal growth, and healing.
All cancers result from some type of alteration in DNA that modi-
¬es how a gene functions. Although certain genetic traits and types of
damage (discussed in the next section) may increase the risk of some
types of cancer, the disease more often arises from random damage to
DNA, combined with or followed by a massive failure of the body™s
innate cancer-surveillance and -control systems. In essence, cancers
develop as a result of a complex interplay of genetics, diet, lifestyle, and
environmental factors. And for as much as we do understand about the
origins of cancer, there is much that we do not understand.
Researchers have found that tracing an inherited risk of cancer can
be a vexing process. The reason is that people often “inherit” (or adopt)
the eating and lifestyle habits of their parents, which are powerful in¬‚u-
ences on the risk of developing cancer. Hundreds, if not thousands, of
factors can come into play in causing a cancer. For example, tobacco
smoke is a well-known carcinogen, but not every smoker develops can-
cer. The reason is that some people, for genetic reasons, are far better
than others at breaking down and disposing of toxins. Diet interacts
with these factors”some foods, such as cruciferous vegetables, contain
vitamin-like substances that enhance the body™s ability to detoxify and
neutralize tobacco smoke, smog, alcohol, pesticides, and other haz-


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