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ardous chemicals.
Most cancer-causing mutations form in one of two ways. One
results from free-radical damage to DNA, which accumulates with age
and also explains why the risk of cancer increases with age. The other
results from nutritional de¬ciencies, particularly of folic acid and other
B vitamins, which are needed for DNA production and repair and for
maintaining overall genetic stability.The effect of an outright de¬ciency
of one or more B vitamins, which may affect 10 to 20 percent of Amer-
icans, is comparable to being exposed to radiation from a nuclear
bomb. DNA literally breaks apart, preventing genes from functioning
168 F E E D YO U R G E N E S R I G H T


normally. Furthermore, a lack of B vitamins, as discussed in chapter 5,
prevents the normal suppression of cancer-causing oncogenes.
Aside from their random damage to DNA throughout the body,
free radicals and nutrient de¬ciencies also increase the likelihood of
mutations in genes speci¬cally related to cancer risk. Once cancers
form, their growth can be promoted by emotional factors and hor-
mones. Cancers also generate large numbers of their own free radicals,
creating a condition that spawns further mutations in cancer cells, often
making at least some of them resistant to conventional medical
chemotherapy and radiation therapy.

The Gene Connection
TUMOR-SUPPRESSION GENES
Researchers have so far identi¬ed an estimated seventeen hundred
oncogenes”that is, genes that appear to be involved in initiating or
promoting cancer growth. These genes, as well as cancer-causing muta-
tions in DNA, are suppressed through a variety of mechanisms. One of
these mechanisms is DNA methylation, which depends on folic acid
and other B vitamins.
Several genes have been identified as having specific cancer-
suppressing roles. Of these the p53 gene (which programs protein 53) is
the best understood. The p53 gene plays a key role in inhibiting cancer-
cell growth, but the gene can become ineffective when it is mutated.
Defective p53 genes have been identi¬ed in more than ¬fty types of
cancer”including about 30 percent of breast cancers, 50 percent of
brain cancers, and 90 percent of cervical cancers. In rare cases defective
nonfunctioning p53 genes are inherited, leading to an increased risk of
cancer among most members of the same family. Folic acid and sele-
nium help maintain the normal activity and genetic stability of p53.
Meanwhile, the GST gene codes for several types of glutathione-
S-transferases, enzymes that play important roles in preventing cancer.
Glutathione-S-transferases function as antioxidants that protect
against free-radical damage, and they also aid the body™s breakdown of
hazardous chemicals. However, researchers have estimated that half of
white and about one-third of African Americans in the United States
have defective versions of the GST gene. In one study, researchers
found that the GST gene was absent in four out of ¬ve women with
gliomas, a type of brain cancer. Polymorphisms in the GST gene have
also been linked to in¬‚ammatory diseases and allergic reactions to air
pollutants, such as diesel exhaust.
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VITAMIN D RECEPTOR (VDR) GENE
The VDR gene codes for the vitamin D receptor, which in¬‚uences how
ef¬ciently the body uses vitamin D. Researchers have identi¬ed a vari-
ety of VDR polymorphisms, and some polymorphisms have been
strongly associated with an increased risk of breast, prostate, and colon
cancer. Considerable pharmaceutical research is under way to develop
synthetic vitamin D molecules that might be effective anti-cancer
drugs. (See further discussion of the VDR gene in “The Vitamin D
Quandary” section of this chapter.)

BREAST CERVICAL CANCERS
AND
In a typical year, approximately 200,000 women in the United States
will be diagnosed with breast cancer, and about 45,000 will die from it.
Despite exhaustive research, only a handful of genes have been linked
to an increased risk of breast or cervical cancers. The risk associated
with these genes must be seen in the proper context: while having one
of these genes increases a woman™s lifetime risk of breast cancer, not
every woman with the gene will in fact develop breast cancer.
Of these genes, BRCA1 and BRCA2 are the best known and most
studied. However, assessing the risk posed by the BRCA1 and BRCA2
genes is a little like entering a statistical jungle. In the United States,
one or both of these genes are found in fewer than 0.5 percent of
women overall but are found in about 2.5 percent of Jewish women of
Eastern European heritage. Although BRCA1 and BRCA2 are com-
monly described as breast-cancer genes, they normally serve important
functions in lactation and cancer-cell suppression. Normal turns to
abnormal when the BRCA1 or BRCA2 genes are mutated, and there
is evidence that these genes are inherently unstable and prone to dam-
age. Having mutations in BRCA1 and BRCA2 genes increases a
woman™s risk of breast cancer by 60 to 85 percent and cervical cancer
by 15 to 40 percent. In the end, mutations in these genes account for
only about 2 percent of all breast cancers.
Researchers also believe that the CHEK2 gene is associated with
an increased risk of breast cancer. CHEK2 is involved in recognizing
and repairing DNA damage and preventing cancer. However, muta-
tions in the CHEK2 gene have been identi¬ed in 4.2 percent of women
diagnosed with breast cancer and who also had a strong family predis-
position of developing the disease. While the CHEK2 mutation mod-
estly increases the risk of breast cancer in women, men with the
mutated gene have a tenfold greater risk of developing breast cancer.
170 F E E D YO U R G E N E S R I G H T


Again, the vast majority of breast-cancer cases have not been associ-
ated with any speci¬c type of genetic mutation or defect.

PROSTATE CANCER
Some 189,000 men in the United States are diagnosed with prostate
cancer, and 30,000 die from the disease each year. While several genes
have been associated with prostate cancer, the links are not particularly
strong. Rather, certain dietary and lifestyle factors increase the risk of
genetic damage in prostate cells, setting the stage for prostate cancer.
The hereditary prostate-cancer gene (HPC1) has been studied the
most, although its association with prostate cancer has not been con-
sistent. Several other genes involved in the metabolism of male hor-
mones have also been associated with prostate cancer, but none seems
to play a dominant role.
Rather, as in cancer in general, it appears that a variety of muta-
tions, accumulating over several decades, increase the risk of prostate
cancer. These mutations are likely the result of chronic prostate infec-
tion or in¬‚ammation, such as prostatitis, which generates large numbers
of free radicals. The risk is compounded by a diet low in protective
antioxidants and high in fat. Indeed, research has consistently shown
that consumption of antioxidant-rich vegetables and fruits lowers the
risk of prostate cancer, whereas diets high in red meats and fats
increase the risk.

What You Can Do
Medical testing for the presence of some cancer-associated genes is
available, but it is expensive. For example, genetic testing for BRCA1
and BRCA2 costs about three thousand dollars, though some insurers
will cover this cost if a woman has a strong family risk of developing
breast cancer. However, bear in mind that the absence of these genes
may provide a false sense of security about having a low likelihood of
developing breast or cervical cancer.

DIET
Your best chance of reducing your risk of cancer is through a combi-
nation of diet, supplements, and lifestyle. Hundreds of scienti¬c studies
have shown that people eating diets high in vegetables and fruits have
a relatively low risk of most cancers. Follow the dietary guidelines
described in chapter 7, with an emphasis on nonstarchy vegetables,
fruit, ¬sh, and culinary herbs. Herbs are rich sources of a wide variety of
171
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antioxidants, and garlic, as an example, has been shown to protect DNA
from damage.

SELENIUM
Selenium forms part of several glutathione peroxidase compounds,
among the body™s most powerful antioxidants. If you do not obtain ade-
quate dietary selenium, your body will not be able to make these
antioxidants. Like other antioxidants, these glutathione peroxidases
help prevent free-radical damage to genes, which can increase the risk
of cancer.
In a landmark study of 1,300 men and women, people who took 200
mcg of selenium daily for an average of four and a half years bene¬ted
from signi¬cant reductions in the risk of several cancers. Selenium sup-
plements lowered the risk of prostate cancer by 63 percent, colorectal
cancer by 58 percent, and lung cancer by 46 percent, according to a
report in the Journal of the American Medical Association. A separate
study, conducted at the Fred Hutchinson Cancer Research Center in
Seattle, found that patients with high blood levels of selenium had
about half the risk of developing precancerous cell changes in the
esophagus.

VITAMIN E
In a review of ¬fty-nine studies on vitamin supplements and cancer risk,
Ruth E. Patterson, Ph.D., of the University of Washington found that
vitamin E was most consistently linked to a low cancer risk. In one study,
relatively small amounts of supplemental vitamin E (50 IU daily) low-
ered the risk of prostate cancer by 48 percent over a nine-year period.
In cell and rodent research, the natural succinate form of vitamin E
(d-alpha tocopheryl) appears to have potent anticancer effects, far
beyond those of other forms of vitamin E. It works in part by inducing
apoptosis (self-destruction) of cancer cells, but it does not harm normal
cells. Kedar N. Prasad, Ph.D., of the University of Colorado has reported
that vitamin E succinate inhibits the growth of many different types of
cancer cells, including those of the breast, prostate, colon, and skin.
Research has also shown that vitamin E succinate enhances the effects
of radiation, chemotherapy, and hyperthermia in killing cancer cells.

FOLIC ACID
This B vitamin, along with vitamins B6 and B12, helps maintain normal
DNA-repair processes and suppresses the activity of cancer-promoting
172 F E E D YO U R G E N E S R I G H T


oncogenes. Low levels of these nutrients lead to “genome instability”
and increase the risk of cancer.

COENZYME Q10
Women with breast cancer and noncancerous breast lesions commonly
have low blood levels of coenzyme Q10, a vitamin-like nutrient.
Although CoQ10 functions as a protective antioxidant, its anticancer
properties seem more related to boosting the activity of immune cells
to ¬ght cancer.
In several journal articles, Dr. Knud Lockwood reported the use of
high doses of CoQ10 (390 mg daily) to prevent the recurrence of breast
cancer in women. Lower dosages did not provide consistent bene¬ts.
CoQ10 may have particularly important functions in the prevention of
breast cancer, although this has not yet been studied.

LYCOPENE
In the mid-1990s Dr. Edward Giovannucci of Harvard University
reported that men eating ten or more weekly servings of tomato sauces
were 45 percent less likely to develop prostate cancer. Tomatoes are
rich in lycopene, a potent antioxidant that concentrates in the prostate.
A later report by Giovannucci described ¬fty-seven human studies in
which tomatoes were associated with a lower risk of lung, breast,
esophagus, and colon cancers.
Relatively few studies have been conducted on pure lycopene, and
the research suggests that the active components consist of lycopene
and other carotenoids found in whole tomatoes and sauces.These other
carotenoids include phytoene, gamma-carotene, neurosporiene,
phyto¬‚uene, beta-carotene, and zeta-carotene.
In a recent study, Dr. Omer Kucuk of Wayne State University in
Detroit used a lycopene-rich tomato extract to signi¬cantly reduce the
size of prostate cancer tumors. He asked 15 men with recently diag-
nosed prostate cancers to take a tomato extract (containing 30 mg of
lycopene, plus other tomato antioxidants) daily for three weeks before
surgery. After surgery the prostates of these men were compared with
those of 11 men who did not receive supplements before surgery.
Lycopene reduced the size of the men™s tumors and blocked the can-
cer™s invasive metastasis of other tissues. Eighty percent of the men tak-
ing lycopene supplements had relatively small tumors, compared with
fewer than half of the men not receiving the supplements. In addition,
73 percent of men taking lycopene had tumors con¬ned to the prostate,
compared with only 18 percent of the nonsupplemented group.
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COMBINING ANTIOXIDANTS CHEMOTHERAPY
WITH
Some nutritionally oriented physicians have also used large dosages of
vitamins and minerals to treat cancers, often in conjunction with or
after conventional medical therapies. Dr. Jeanne Drisko of the Uni-
versity of Kansas Medical Center has successfully treated cases of cer-
vical cancer with daily dosages of vitamin E (1,200 IU), coenzyme Q10
(300 mg), vitamin C (9 grams), beta-carotene and mixed carotenoids
(25 mg), and vitamin A (10,000 IU). The regimen includes intravenous
vitamin C (60 grams twice weekly), as well as conventional chemo-
therapy. These nutrients do not directly affect tumors. Rather they
boost the ability of the body™s many different immune cells to attack
the cancers.
As you might imagine, many other factors in¬‚uence the growth of
cancers. High levels of some hormones, such as estrogen (estradiol),
testosterone, and insulin are known to promote cancer growth. Living
in cities with significant air pollution, using tobacco products, and
drinking excessive amounts of alcohol also increase the risk of cancer”
mainly by increasing free-radical mutations to DNA. In addition, cer-
tain chronic emotional states, such as depression, can increase the risk
of cancer, mostly likely because of underlying alterations in DNA
methylation.


Cardiovascular Diseases
What Happens
Coronary artery (heart) disease is the leading cause of death among
Americans and other Westerners. Stroke, a type of cardiovascular dis-
ease affecting blood vessels in the brain, is the third leading cause of
death. Each year in the United States, approximately 700,000 people
die from heart disease and 160,000 die from stroke.
In general, coronary heart disease is characterized by an abnormal
thickening of the inner walls of arteries within the heart, which reduces
blood ¬‚ow. The heart, like every other organ, depends on a steady sup-
ply of oxygen and nutrients, which are delivered via the bloodstream.
An interruption of blood ¬‚ow to the heart causes what is popularly
known as a heart attack. The most common type of stroke, called an
ischemic stroke, follows a similar pattern in that it is caused by a block-
age in a blood vessel that interrupts blood ¬‚ow to the brain. Hemor-
rhagic strokes, a less common type of stroke, result from the rupture of
a blood vessel in the brain.
174 F E E D YO U R G E N E S R I G H T


The Gene Connection
Researchers have identi¬ed several speci¬c genetic variations that can
predispose people to cardiovascular disease. However, the risk posed
by these genes can almost always be offset through healthier eating
patterns and lifestyle habits. Furthermore, it appears that most cases of
cardiovascular disease result from more generalized and extensive
damage to genes and nongene cell structures, which ultimately impair
normal heart function. While much of this damage is age-related”that
is, acquired slowly over many years”the rate of gene damage to heart
cells can be slowed signi¬cantly.
People who inherit one or two copies of genes (from one or both
parents) that program for an inef¬cient form of methylenetetrahydro-
folate reductase (MTHFR), an enzyme essential for folic acid utiliza-
tion, have an increased risk of suffering a heart attack or ischemic
stroke. This defect is technically known as the MTHRF 677 C’T geno-
type. Although it can be tested for, it is usually far easier simply to
measure blood levels of homocysteine and then to interpret the results
with a physician.
Elevated homocysteine levels, a recognized risk factor for heart
disease and stroke, directly damage cells forming blood vessel walls,
setting in motion a series of events leading to the deposition of choles-
terol. Homocysteine is also a sign of poor methylation, suggesting that
the body™s production and regulation of DNA activity is impaired.
An extremely high homocysteine level indicates that you are not prop-
erly utilizing folic acid, because of either low dietary intake or a genetic
polymorphism. Either way the remedy is the same: eating more
leafy green vegetables (rich in folic acid) and taking a high-potency
B-complex vitamin supplement.
Some people have variations in a gene that programs one of the
body™s cholesterol-transporting proteins. For example, people with an
inef¬cient APOE E4 variation of the apoliprotein gene, which is rela-
tively common in some parts of Scandinavia, tend to have higher
blood-cholesterol levels and are more likely to suffer a heart attack. In
contrast, the APOE E2 variation of the gene, common in Japan, pro-
grams for a very ef¬cient form of apoliprotein, which helps maintain
low levels of cholesterol and reduces the risk of a heart attack.
Another important factor comes into play with cholesterol, and
that is the susceptibility of low-density lipoprotein (LDL) to free-
radical-induced oxidation. Such oxidation is more likely to occur when
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people consume large amounts of polyunsaturated fats (found in most
cooking oils and fried foods), which increase vitamin E requirements.
Oxidized LDL, but not normal LDL, triggers an inflammatory
immune response known to be an early step in the development of
heart disease. During this immune response, white blood cells seek out
and capture oxidized LDL globules, and then the LDL-loaded white
blood cells become lodged in blood vessels, where they release free
radicals and damage the blood vessel walls.These free radicals circulate
in heart cells, causing genetic damage and accelerating the aging of
heart cells.
Some people suffer from familial hypercholesterolemia, an inher-
ited condition that causes extreme elevations of cholesterol and other
blood fats and a greater risk of premature coronary artery disease.
Many studies have found that supplemental vitamins E and C, or the
addition of plant sterols (plant extracts found in supplements and some
margarines), can lower cholesterol levels in children and adults with
familial hypercholesterolemia and, presumably, reduce their long-term
risk of heart disease.
A study published in the January 1, 2004, issue of the New England
Journal of Medicine shed further light on the role of genetic defects and
in¬‚ammation in heart disease. James H. Dwyer, Ph.D., of the University
of Southern California in Los Angeles and his colleagues investigated
speci¬c genetic polymorphisms, signs of heart disease, and measures of
inflammation in 470 middle-aged men and women. Dwyer focused
speci¬cally on polymorphisms in the ALOX5 gene programming for
5-lipoxygenase, an enzyme involved in the body™s production of in¬‚am-
mation-promoting molecules.
Genetic testing found that 6 percent of the subjects had polymor-
phisms in the ALOX5 gene, and these variations were associated with
two signs of heart disease: a narrowing of the internal diameter of
blood vessels and a doubling of C-reactive protein levels, an indication
of low-grade in¬‚ammation in the heart. However, the polymorphisms
in the ALOX5 gene did not by themselves lead to heart disease. Rather
the subjects™ diets strongly in¬‚uenced their risk. People whose diets
were rich in linoleic acid (found in corn, saf¬‚ower, and other common
cooking oils) and arachidonic acid (made in the body from linoleic
acid) were far more likely to have signs of heart disease. In contrast,
people who consumed more omega-3 fats, found in fresh (nonbreaded,
nonfried) ¬sh, did not have signs of heart disease.
176 F E E D YO U R G E N E S R I G H T


What You Can Do
From a dietary standpoint, emphasize nutrient-dense foods, particu-
larly wild, cold-water ¬sh and fresh, steamed, or stir-fried vegetables.
Recent research has con¬rmed that reducing dietary carbohydrates”
starches and sugars”is far more effective than avoiding saturated fat in
improving cardiovascular risk factors. If you avoid vegetables, you risk
increasing your homocysteine levels.

B VITAMINS
An ideal homocysteine level is less than 6 micromoles per liter of
blood. As homocysteine levels increase, so does your risk of heart
attack and stroke, and homocysteine levels above 13 mmol/L indicate
a serious risk. In most people homocysteine levels can be decreased by
taking 400 to 800 mcg of folic acid daily. However, it is better to take a
high-potency B-complex or multivitamin supplement that includes at
least 50 mg of vitamin B6 and 100 mcg of vitamin B12. Although ele-
vated homocysteine levels are usually directly linked to folic acid lev-
els, inadequate amounts of these other B vitamins can also result in
excess homocysteine.

VITAMIN E
Some research has shown that the deleterious effect of the APOE E4
gene can be prevented with vitamin E. In addition, vitamin E helps pre-
vent the oxidation of LDL, which is a more serious problem than mod-
erately elevated LDL or total cholesterol. Unfortunately, LDL
oxidation is rarely measured outside of university research settings.
For most people 200 to 400 IU of vitamin E daily should be suf¬cient.
If you have elevated LDL or total cholesterol, consider supplementing
with 400 to 800 IU. With higher cholesterol levels, your vitamin E lev-
els increase because you need more relative to the greater amount of
cholesterol. Also, if you have made a habit of eating a lot of fried foods
(burgers, fried chicken, french fries), the extra vitamin E will help
reduce oxidation from the consumption of fried oils. Supplemental
vitamin C (1,000 mg) daily will also be bene¬cial.
Selecting a vitamin E product can be confusing. Natural vitamin E
is absorbed into the blood and tissues twice as ef¬ciently as are syn-
thetic forms. Therefore it makes sense to purchase natural-source vita-
min E. Natural vitamin E will be identi¬ed in ¬ne print on the label as
d-alpha tocopherol, d-alpha tocopheryl acetate, or d-alpha tocopheryl
succinate. (Synthetic is identi¬ed as dl-alpha.) Some natural vitamin E
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products include other types of vitamin E molecules, such as mixed
tocopherols and tocotrienols. The natural d-alpha form provides the
lion™s share of vitamin E™s antioxidant properties, but the other forms
may also be worthwhile.
Other antioxidants, such as vitamin C and coenzyme Q10, have also
been shown to reduce LDL oxidation. Several studies have shown strong
relationships between vitamin C intake and longevity, as well as a lower
risk of stroke. Vitamin C is essential for the body™s manufacture of heart
cells and for maintaining the structure and ¬‚exibility of blood vessels.

FATTY ACIDS
In my earlier book, The In¬‚ammation Syndrome, I detailed the rela-
tionship between in¬‚ammation and heart disease. Over the past few
years, medicine has largely recognized heart disease as an in¬‚ammatory
disorder of blood levels. As con¬rmed by the above-mentioned study
on the ALOX5 gene, some nutrients have a decidedly proin¬‚ammatory
effect on heart disease, arthritis, allergies, and many other diseases.
Processed foods, rich in common cooking oils and re¬ned carbohy-
drates, provide excessive quantities of the nutrients involved in the
body™s in¬‚ammatory response. In contrast, omega-3 ¬sh oils, in either
cold-water ¬sh (such as salmon, herring, and tuna) or supplements,
have a decidedly antiinflammatory effect. Other nutrients, such as
gamma-linolenic acid (found in borage, evening primrose, or black cur-
rant seed supplements), oleic acid (found in olive oil), and antioxidants
also enhance the body™s native antiin¬‚ammatory processes.
Your individual risk of cardiovascular diseases is also the result of a
great many factors besides diet, which ultimately help maintain normal
gene function or cause gene damage. Smoking tobacco products gener-
ates large quantities of free radicals, which damage the heart, lungs, and
other organs. Antioxidant supplements can reduce some of the damage,
but not all of it. Being overweight increases the risk of heart disease, as
do chronic psychological stress and a sedentary lifestyle. Each of these
risk factors”even those with a genetic basis”are modi¬able.



Cardiomyopathy and Heart Failure
What Happens
The heart is a muscle, and cardiomyopathy is a weakening of this muscle,
which reduces the heart™s ability to pump blood. Cardiomyopathy is
178 F E E D YO U R G E N E S R I G H T


different from the more common coronary artery disease, in which a nar-
rowing of blood vessel walls reduces the ¬‚ow of blood within the heart.
Idiopathic dilated cardiomyopathy is characterized by an enlarge-
ment and thinning of the heart muscle, which reduces heart function. It
accounts for about 80 percent of all cardiomyopathy cases. Hypertrophic
cardiomyopathy results from a thickening and stiffening of the heart
muscle, which reduces heart function. It accounts for about 20 percent of
all cardiomyopathy cases. Heart failure, in which the heart cannot pump
suf¬cient blood to nourish the body with oxygen and nutrients, can result
from either cardiomyopathy or coronary artery disease.

The Gene Connection
The heart, which beats approximately a hundred thousand times daily,
has enormous energy requirements. Healthy heart cells are rich in
mitochondria and the energy-promoting nutrients described in chapter
4, including coenzyme Q10, alpha-lipoic acid, and carnitine. While car-
diomyopathy can result from rare inherited genetic defects, it is more
commonly the result of acquired genetic damage or a severe depletion
of mitochondrial nutrients without genetic damage.
In some cases viral infections lead to myocarditis, an in¬‚ammation
of the heart muscle. Such viral infections can disrupt the DNA in heart
cells and lead to the deaths of large numbers of heart cells. Melinda
Beck, Ph.D., of the University of North Carolina at Chapel Hill and
Orville Levander, Ph.D., of the U.S. Department of Agriculture have
shown that infection with the coxsackie virus, a common cause of sore
throats and coldlike symptoms, combined with selenium de¬ciency, can
lead to a viral infection of the heart and heart failure.
Heart failure can also be induced by cholesterol-lowering “statin”
drugs, including atorvastatin, lovastatin, prevastatin, and simvastatin.
Statins inhibit a key enzyme involved in the body™s production of cho-
lesterol. However, the same enzyme is also necessary for the body™s
production of coenzyme Q10, a vitamin-like substance that plays a cru-
cial role in producing energy in heart cells. So when statin drugs block
the body™s production of cholesterol, they also reduce the production
of CoQ10.

What You Can Do
Age-related damage to mitochondrial DNA can be a cause of
cardiomyopathy and heart failure. However, in many cases cardio-
myopathy and heart failure stem from an extreme depletion of
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energy-promoting nutrients. This depletion can be the result of diets
high in re¬ned and processed foods, which fail to provide crucial nutri-
ents or the building blocks of those nutrients.

COQ10
Also known as ubiquinone, CoQ10 is found in every cell of the body,
though people with cardiomyopathy and heart failure typically have
low levels of it. It is not surprising that replenishing CoQ10 improves
heart function in these patients. In one typical study, researchers used
CoQ10 supplements to treat 11 heart failure patients who were likely
candidates for transplant surgery. All of the patients improved, some
regaining normal heart function without any other medications. More
recently, in Molecular Aspects of Medicine, Dr. Peter Langsjoen
reported 200 mg of CoQ10 daily helpful in the treatment of hyper-
trophic cardiomyopathy, which is characterized by a thickening and
stiffening of the heart muscle. Therapeutic amounts typically range
from 240 to 360 mg daily in divided doses.

CARNITINE
A component of protein, carnitine helps transport fats into mitochon-
dria, where they are burned for energy. It also regulates the use of
coenzyme A, an energy-producing compound built around the B vita-
min pantothenic acid. Dr. Ioannis Rizos of the University of Athens
Medical School studied 70 patients who took either 2 grams of carni-
tine or a placebo daily for three years. The patients suffered from heart
failure resulting from dilated cardiomyopathy. Those who took carni-
tine had a much better rate of survival compared with those taking the
placebo. Over the course of the three-year study, 6 of the patients tak-
ing the placebo died, whereas all but 1 of the patients taking carnitine
survived. In addition, only 1 patient in the carnitine group developed
arrhythmias, compared with 7 in the placebo group. Try 2 grams daily in
divided doses.

VITAMIN B 1
Patients with heart failure are commonly deficient in vitamin B1
(thiamine), needed for several key energy-producing chemical reac-
tions. This de¬ciency can be exacerbated with diuretic drugs used to
treat symptoms of heart failure. Several studies have found that vitamin
B1 can improve heart function in patients with heart failure. For
example, Dr. David Ezra of the Sheba Medical Center in Israel
reported that both oral supplements and intravenous vitamin B1
180 F E E D YO U R G E N E S R I G H T


corrected de¬ciencies induced by the drug furosemide (used to treat
heart failure) and improved the pumping action of the patients™ hearts.
Try 100 to 200 mg daily in divided doses.


Celiac Disease
What Happens
Celiac disease is an inherited intolerance of gluten, a family of related
proteins found in wheat, rye, barley, and many other grains. In the dis-
ease™s most recognized form, gluten proteins trigger an autoimmune
response that attacks the intestinal wall. As the surface of the intestinal
wall decays, digestion becomes impaired, and the resulting malnutrition
frequently leads to anemia and osteoporosis. However, celiac disease
often progresses for many years without obvious symptoms, or without
physicians™ linking symptoms to it.
This deterioration of the digestive tract sometimes leads to “leaky
gut syndrome,” in which undigested proteins enter the bloodstream
and trigger a variety of symptoms resembling food allergies. Other
common symptoms of celiac disease include bloating, diarrhea, der-
matitis, fatigue, and migraine headaches. In fact, researchers have
reported that celiac disease may be intertwined in approximately 250
diseases, including depression, dermatitis herpetiformus, treatment-
resistant iron-de¬ciency anemia, Down syndrome, irritable bowel syn-
drome, lactose intolerance, multiple vitamin and mineral de¬ciencies,
hypothyroidism, and schizophrenia.
Recent studies have found that celiac disease has been widely under-
diagnosed. Because it can cause so many different symptoms, some
researchers have referred to it as a “clinical chameleon.” By new esti-
mates it may affect approximately one in a hundred Americans and
Northern Europeans. Some researchers have estimated that a more gen-
eralized form of gluten intolerance, without all the intestinal symptoms
of classic celiac disease, may affect almost one-half of the population.
Unfortunately, the estimated prevalence of celiac disease and non-
celiac gluten intolerance is confounded by two factors. First, many peo-
ple who carry the genes for celiac disease do not develop any signs or
symptoms of the disease, which suggests that other unidenti¬ed genes
or environmental factors may be involved. Second, people without a
genetic predisposition for gluten intolerance may develop symptoms of
celiac disease. The latter situation might be partly explained by the
presence of another family of proteins, called lectins, found in wheat
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and many other grains, which can also trigger abnormal autoimmune
reactions. For example, lectin sensitivity has been found in some causes
of rheumatoid arthritis.

The Gene Connection
Celiac disease and other forms of gluten intolerance serve as good
illustrations of how genes and diet interact. Many thousands of years
ago, the HLA-DQ2 and HLA-DQ8 genes, which predispose a person
toward celiac disease, were relatively common among humans. During
most of human evolution, these genes posed no disadvantage, because
people rarely if ever consumed grains. This situation changed approxi-
mately ten thousand years ago, when people began cultivating gluten-
containing grains.
Once the widespread consumption of gluten-containing grains
become common, the incidence of many diseases skyrocketed. The
result was that the HLA-DQ2 and HLA-DQ8 genes were being turned
on, as were abnormal immune responses. Archaeological evidence
from about ten thousand years ago indicates significant postgluten
increases in birth defects, osteoporosis, arthritis, rickets, dental enamel
defects, infertility, child mortality, and disease and death at all ages. The
reductions in fertility and increases in childhood mortality served to
reduce the numbers of people carrying the HLA-DQ2 and HLA-DQ8
genes.
Today genetic testing can identify the presence of the HLA-DQ2
gene, which is found in 90 to 95 percent of celiac patients, and the
HLA-DQ8 gene, found in 5 to 10 percent of cases. In addition, your
physician or gastroenterologist can draw blood to test for IgG and IgA
antigliadin antibodies, a worthwhile initial screening for celiac disease.
More speci¬c tests for gluten sensitivity include the antitissue transglu-
taminase (anti-tTG) and IgA antiendomysial tests. A stool test for
gluten sensitivity is available, and intestinal biopsies can reveal the
extent of intestinal damage from years of eating gluten-containing
grains.
A study published in the February 2004 issue of the Journal of
Pediatric Gastroenterology and Nutrition signi¬cantly expanded our
understanding of the genetic implications of celiac disease. A team of
researchers found that genetic damage decreased when children with
celiac disease began eating a gluten-free diet. After two years on a
gluten-free diet, children with celiac disease showed levels of genetic
damage not significantly greater than that in healthy children. The
182 F E E D YO U R G E N E S R I G H T


researchers theorized that the “genomic instability” in untreated celiac
disease was a consequence of chronic intestinal in¬‚ammation.

What You Can Do
Celiac disease and more generalized gluten intolerance represent a
widespread genetic incompatibility with commonly consumed gluten-
containing grains. The irony is that they are the principal source of
dietary carbohydrates in the United States, Europe, South America,
and many other parts of the world.
There are no drugs to treat celiac disease and gluten sensitivity.
Rather, the treatment is entirely dietary. Like it or not, people with
celiac disease must avoid all gluten-containing foods for the rest of
their lives. Complete avoidance of gluten is particularly important in
cases of “silent” celiac disease, in which the damage is primarily to the
intestine and the consequences (such as osteoporosis) may not be obvi-
ous for many years. People with celiac disease must not eat breads,
hamburger buns, cereals, pastas, muf¬ns, cookies, pizza, or any ¬sh or
chicken dredged in wheat flour. Furthermore, they must learn to
become careful readers of food labels for the mention”or mere hint”
of a gluten-containing grain. It may be worthwhile as well to avoid
dairy products, because lactose intolerance and sensitivity to casein (a
protein found in dairy products) is often associated with gluten intol-
erance.
Because of the dietary restrictions, many people diagnosed with
celiac disease become resentful or depressed when they cannot con-
tinue to consume processed foods, fast foods, or junk foods with aban-
don”and suffer the same risk of obesity and diabetes as the rest of the
population. Some gluten-free substitutes, such as rice-based breads or
pastas, are available at health food stores, but these provide mostly
empty carbohydrate calories. In fact, people with celiac disease often
come to believe that any gluten-free food is good to eat. However,
“gluten-free” often means “nutrient-free,” as in the case of gluten-free
but highly re¬ned breads, pastas, and cookies.
Other than relieving symptoms of celiac disease, gluten-free
carbohydrates are no better than gluten-containing carbohydrates for
your overall health. Because they tend to consist of highly refined
carbohydrates (often from potato or rice) and sugars, they can increase
the risk of obesity, Syndrome X, diabetes, and heart disease. A much
more sensible and nutritionally sound approach would be to limit car-
bohydrate intake while focusing on wholesome, nutrient-dense foods,
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such as chicken, turkey, ¬sh, and nonstarchy vegetables and fruits. This
approach would be consistent with our ancient pregrain dietary
habits”and with the recommendations in this book.


Depression and Moodiness
What Happens
Depression and moody behavior, including a tendency toward irri-
tability and anger, have a combination of psychosocial and nutritional
roots. In some people the triggering event could be the end of a rela-
tionship, the death of a loved one, or working at a stressful job, all
situations that can profoundly influence eating habits, normal bio-
chemistry, and gene expression in brain cells. Conversely, certain
genetic traits and nutritional and biochemical imbalances can increase
a person™s susceptibility to depression and moodiness.
Depression, which affects about 20 million Americans in varying
degrees, is usually characterized by a profound sense of sadness and
hopelessness”the belief that life will not get better. Mild to moderate
depression can be treated with both natural and pharmaceutical meth-
ods, whereas severe depression is typically very resistant to any treat-
ment. More common “everyday” mood disorders, such as “down” days,
irritability, impatience, anger, and hostility, affect millions of people to
varying degrees.

The Gene Connection
Some genetic polymorphisms do increase the risk of depression and
mood disorders. However, the impact of these polymorphisms depends
on diet and stressful events.
As you read in chapter 5, polymorphisms in the gene coding for
methylenetetrahydrofolate reductase (MTHFR) reduce the ef¬ciency
of folic acid metabolism, leading to inef¬cient methylation, elevated
levels of homocysteine, and impaired DNA synthesis and repair. Poly-
morphisms in the MTHFR gene also boost a person™s risk of depres-
sion. The reason is that methylation, which depends on folic acid,
vitamin B6, and other nutrients, feeds into the body™s production of
neurotransmitters, such as serotonin and taurine. Researchers have
found that middle-aged women with elevated homocysteine levels, a
sign of poor methylation, are twice as likely to be depressed, compared
with women who have normal homocysteine levels.
In addition, polymorphisms in the gene that programs a serotonin-
184 F E E D YO U R G E N E S R I G H T


transport protein can also in¬‚uence susceptibility to depression. One
version of the gene codes for a very ef¬cient serotonin transporter,
whereas the other codes for a poor transporter. People with the inef¬-
cient serotonin-transporter gene are far more likely to experience pro-
longed depression after a stressful event.
Similarly, people who are genetically predisposed to make and
excrete a chemical known as kryptopyrrole are stress-intolerant and
highly susceptible to depression, fatigue, lethargy, and schizophrenia.
(See “Pyroluria” in this chapter.) Kryptopyrrole binds to vitamin B6
and zinc, resulting in increased excretion of these nutrients, and behav-
ioral manifestations of this double de¬ciency are common.

What You Can Do
DIETARY CONSIDERATIONS
Low blood sugar”more accurately described as rapid and unpre-
dictable drops in blood-glucose levels”can impair cognitive function
and alter moods, increasing feelings of impatience, irritability, anger,
and hostility. You might think that eating sugary foods would be the
fastest way to elevate blood-glucose levels, but the opposite is true.
Sugary foods and refined carbohydrates, which the body quickly
breaks down into glucose, brie¬‚y raise glucose levels and improve
moods. But the surge in glucose triggers the secretion of insulin, which
overcompensates in decreasing glucose levels, continuing a vicious
cycle.
Foods high in protein (chicken, turkey, ¬sh, lean meats) or ¬ber
(nonstarchy vegetables) stabilize glucose and insulin levels. The bene-
¬ts are swift. Eating a low-glycemic breakfast”that is, a breakfast that
causes a minimal increase in glucose and insulin”will stabilize blood
glucose up to lunchtime, providing you do not indulge in a high-sugar
midmorning snack.

B VITAMINS
According to David Benton, Ph.D., of the University of Wales, the ear-
liest signs of nutritional de¬ciencies, presuming one pays attention, are
behavioral. In his research Benton has found that vitamin B1 and a
high-potency multivitamin produce striking improvements in mood
among otherwise healthy young adults. Additional research has shown
that folic acid and vitamins B6 and B12 increase MTHFR activity, lead-
ing to higher production of neurotransmitters and improvements in
depression, premenstrual anxiety, and irritability.
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ST. JOHN™S WORT
Several clinical studies have found that St. John™s wort is as effective as
Prozac and Zoloft in treating mild to moderate depression. The herb
also causes fewer side effects than the drugs. In addition, St. John™s wort
also boosts the liver™s detoxi¬cation processes, which has advantages
and disadvantages. The herb helps the body break down toxic chemi-
cals, such as pollutants, but it also speeds the body™s breakdown of
many medications, requiring an adjustment in the drug™s dosage. If you
currently take an antidepressant medication, work with your physician
in changing its dosage and that of any other medications you take. A
general dosage recommendation for St. John™s wort is 300 mg three
times daily.

5-HTP
A form of the essential amino acid tryptophan, 5-hydroxy-tryptophan
is the chemical precursor to serotonin. Researchers believe that it
increases serotonin levels in the brain, which reduces depression and
anxiety. A bene¬cial dosage is 300 to 400 mg daily.


Fatigue and Chronic Fatigue Syndrome
What Happens
Chronic fatigue syndrome (CFS)”so severe that many people suffer-
ing from it have dif¬culty getting out of bed”affects an estimated 2
million Americans. However, more generalized chronic fatigue and
tiredness, which may affect one-fourth of adult Americans, is the most
common physical complaint physicians hear from their patients. Both
conditions are characterized by persistent tiredness, but CFS is far
more severe and often includes extreme muscle weakness, feelings of
depression, and mental fuzziness.

The Gene Connection
Chronic fatigue syndrome is often precipitated by a ¬‚ulike infection or
a signi¬cant exposure to pesticides. The feeling of being “wiped out”
does not go away. The Epstein-Barr virus (which also causes mononu-
cleosis) is frequently a cofactor in CFS. All viruses are capable of
disabling and rewriting DNA, and it is conceivable that severe viral
infections disrupt the genes governing cellular energy production. A
more speculative theory, but a plausible one, holds that pesticides can poi-
son some of the biochemical pathways involved in energy production.
186 F E E D YO U R G E N E S R I G H T


(Similarly, cyanide kills by almost immediately shutting down mito-
chondrial activity throughout the body.) Depression is often intertwined
in CFS, and it may be the principal symptom of CFS. Feelings of depres-
sion can help sustain fatigue, weakness, and lethargy.
More general chronic fatigue and tiredness (in contrast to CFS) can
have a variety of causes apart from damaged mitochondrial DNA.
Diets high in sugars and re¬ned carbohydrates, bouts of hypoglycemia,
prediabetes and diabetes, low thyroid activity, obesity, psychological
stress, inadequate sleep, and depression can be interconnected with
fatigue. In some cases excess copper levels can depress zinc and result
in fatigue.

What You Can Do
Physicians often use energy-promoting nutrients, such as alpha-lipoic
acid, B vitamins, carnitine, and coenzyme Q10, to treat mitochondrial
myopathies. These same nutrients are often helpful in treating CFS and
chronic fatigue, because they provide the nutritional underpinnings of
biochemicals involved in energy production. Most of these nutrients
are discussed in chapter 4 and elsewhere in chapter 10, so they will be
reviewed only brie¬‚y here.

ALPHA-LIPOIC ACID
Alpha-lipoic acid, a vitamin-like nutrient, works in two principal ways.
It improves the ef¬ciency of insulin, enabling the body to burn more
blood sugar for energy. It also accelerates the energy-producing bio-
chemical reactions within mitochondria, leading to higher ATP levels in
the body and the brain. Dosage: 50 to 300 mg daily.

B VITAMINS
Vitamins B1, B2, and B3 play crucial roles in breaking down glucose and
fat for energy. High intake of carbohydrates increases requirements for
vitamin B1 (needed to make enzymes involved in breaking down car-
bohydrates) and very likely those of the other B vitamins. Patients with
CFS have been shown to have low levels of vitamins B1, B2 , and espe-
cially vitamin B6.
Although technically not a B vitamin, NADH (nicotinamide ade-
nine dinucleotide) is built around vitamin B3 and plays a central role in
cellular energy production. In a study conducted at Georgetown Uni-
versity Medical School, Dr. Joseph Bellanti reported that 10 mg of
NADH daily led to gradual improvements in CFS patients.
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CARNITINE
Carnitine helps transport fats into mitochondria, where they are
burned for energy. In a study of 28 men and women with CFS, Dr.
Audius V. Plioplys of Mercy Hospital and Medical Center in Chicago
reported that 3,000 mg of carnitine daily for eight weeks led to signi¬-
cant improvements in symptoms. Inadequate intake of vitamin C,
needed for the body™s own synthesis of carnitine, can cause fatigue, so
vitamin C may be helpful in dosages of 1,000 mg or more daily.

COENZYME Q10
Like the other nutrients discussed in this section, CoQ10 is essential for
cellular energy production. Some cardiologists use it to treat car-
diomyopathy and heart failure. Dr. Peter Langsjoen has reported that
CoQ10 increased energy levels in otherwise healthy octogenarians.
Dosages range from 30 to 300 mg daily.



Hemochromatosis
What Happens
Hemochromatosis is the most common genetic cause of iron overload.
Although iron is an essential nutrient, high levels can be toxic, though
it may take many years for symptoms to become clinically signi¬cant.
The disease typically affects people of Northern European heritage
and is relatively rare in blacks and Hispanics. More than 1 million
Americans have hemochromatosis, and its prevalence in Britain and
other Northern European countries may be as high as 1 in every 140
people.
Hemochromatosis leads to the excessive storage of iron in the liver,
the endocrine (hormone-producing) glands, and the skin. Diagnosis of
the disease is often missed early in life because symptoms, such as
arthritis, impotence, fatigue, and low thyroid, may be vague and attrib-
uted to other causes. Individual symptoms are often related to the
organs in which iron is stored, which impairs the function of those
organs. For example, excess iron storage in the liver may lead to cir-
rhosis or liver cancer, whereas iron storage in the heart may lead to
cardiovascular disease. More clear-cut symptoms do not usually appear
until after age forty, and these symptoms may also include bronze-
colored skin, diabetes, cardiomyopathy, heart failure, and premature
death.
188 F E E D YO U R G E N E S R I G H T


The Gene Connection
Hemochromatosis is usually caused by a mutation in the HFE gene.
Because of the mutation, the amino acid tyrosine is substituted
for cysteine during the production of hemoglobin. This seemingly
minor change alters the way the body stores iron. The mutation is
referred to as HFE C282Y, because it occurs at position 282 of the
HFE gene.
A second gene mutation, H63D, occurs in a small number of
hemochromatosis patients. It is likely that other genes besides HFE are
involved in iron-storage diseases. Researchers have also identi¬ed signs
and symptoms of hemochromatosis in people without known genetic
markers of the disease, suggesting that either additional genes or
lifestyle factors can also lead to iron overload.
In a blood test, elevated levels of iron or serum ferritin levels may
be suggestive of hemochromatosis. However, additional testing is
required for con¬rmation.
Some evidence suggests that people with hemochromatosis may
have had a survival advantage in ancient times. People with celiac dis-
ease commonly suffer from iron de¬ciency (because of poor absorp-
tion), and the HFE mutation may have ensured that people stored
suf¬cient amounts of iron.

What You Can Do
Although it may sound odd, prophylactic phlebotomy”otherwise
known as bloodletting”is the standard medical treatment for
hemochromatosis. It is an effective way of reducing blood (and subse-
quently liver) levels of iron. Begun early enough, it can reduce the risk
of iron-related disease and premature death, enabling people with the
disease to have normal life expectancies.
Some dietary strategies may also be of bene¬t. In a study of 18
patients with genetically confirmed hemochromatosis, researchers
found that regular consumption of black tea with meals signi¬cantly
reduced iron storage as well as the frequency of bloodletting. The
need for bloodletting might also be reduced by avoiding processed,
iron-forti¬ed foods, including breads and pastas, and iron-containing
vitamin and mineral supplements. Some companies, such as Thorne
Research (www.thorne.com), market iron-free supplements. In addi-
tion, iron from vegetables is absorbed less ef¬ciently than is iron from
meat.
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In¬‚ammatory Diseases
What Happens
Nearly everyone is familiar with the redness, swelling, and pain associ-
ated with in¬‚ammation. In¬‚ammation is a normal process that helps
our bodies ¬ght infections and also initiates healing after an injury.
After that healing, the inflammatory response should subside. In
chronic inflammatory diseases, however, the inflammatory reaction
continues and becomes destructive.
Common inflammatory diseases include rheumatoid arthritis,
osteoarthritis, allergies, and asthma. Increasing research indicates that
most and perhaps all diseases involve excessive inflammation. For
example, coronary artery disease is now considered an in¬‚ammatory
disorder of blood vessels, and high levels of in¬‚ammation have been
identi¬ed in Alzheimer™s disease, cancer, diabetes, obesity, and many
other diseases.

The Gene Connection
During an in¬‚ammatory response, several key transcription proteins,
such as nuclear factor kappa-beta and tumor necrosis factor, turn on
numerous genes involved in in¬‚ammation. Some of these genes code
for cytokines, such as interleukin-6 (IL-6) and C-reactive protein
(CRP), which signal other immune cells to amplify the in¬‚ammatory
response.
At the same time, various types of white blood cells become acti-
vated. These white blood cells use free radicals to destroy bacteria,
virus-infected cells, or damaged cells. Some of these free radicals stim-
ulate genes that program various types of adhesion molecules, which
enable white blood cells to stick to normal cells, again sustaining an
in¬‚ammatory reaction. The cytokines, particularly IL-6 and CRP, signal
cells to increase production of another family of hormonelike proin-
¬‚ammatory molecules, including prostaglandin E2.
Our biology heritage has erred on the side of powerful in¬‚amma-
tory responses, and for good reason. Historically, infections and injuries
have been the principal causes of death. As recently as 1900, infections
were still the leading cause of death in the United States, and even
today they remain the leading cause of death worldwide. To survive,
humans needed an aggressive immune response.
But why doesn™t this inflammatory response turn off after it is
190 F E E D YO U R G E N E S R I G H T


needed? The reason, as I explained in The In¬‚ammation Syndrome, is
that modern re¬ned and processed foods provide large amounts of the
building blocks needed for the body™s in¬‚ammatory response but rela-
tively few of the nutrients required to moderate in¬‚ammatory reac-
tions. Diets rich in the omega-6 family of fats (found in corn oil,
safflower oil, and other common cooking oils) contribute to the
immune response, such as by increasing the antiin¬‚ammatory activity
of the ALOX5 gene. In contrast, the omega-3 fats (found in fish,
¬‚axseed, and leafy green vegetables) lessen the in¬‚ammatory response.
Our ancient diet provided relatively equal and balanced amounts of
these fats. Processed and re¬ned foods provide twenty to thirty times
more of the proin¬‚ammatory omega-6 fats.
In addition, most people eat relatively small amounts of vegetables
and fruits, depriving them of antioxidants that also have antiin¬‚amma-
tory bene¬ts. Together, the large amount of omega-6 fats, combined
with relatively small quantities of omega-3 fats and antioxidants, set the
stage for an unbalanced in¬‚ammatory response and chronic in¬‚amma-
tory diseases.

What You Can Do
As you might expect, the composition of your diet influences the
activity of genes involved in in¬‚ammation. For example, the ALOX5
gene codes for 5-lipoxygenase, an enzyme needed to make
inflammation-promoting molecules. However, this gene™s activity is
regulated in part by the relative amounts of dietary omega-6 and
omega-3 fats. In people consuming large amounts of omega-6 fats, the
ALOX5 gene produces substantial amounts of 5-lipoxygenase and
proin¬‚ammatory compounds. But when the diet is rich in omega-3 fats,
the gene codes for less 5-lipoxygenase and small amounts of proin-
¬‚ammatory substances.
A nutrient-dense diet can be easily tailored to emphasize a variety
of antiin¬‚ammatory foods. Cold-water ¬sh, such as wild salmon, is par-
ticularly rich in antiin¬‚ammatory omega-3 fats, and it can be baked in
olive oil, which contains antiin¬‚ammatory omega-9 fats. The ¬sh can be
served with nonstarchy vegetables, such as cauli¬‚ower and broccoli,
which contain inflammation-suppressing antioxidants. Such an anti-
in¬‚ammatory diet should avoid or strictly limit consumption of re¬ned
carbohydrates and sugars, because these foods lead to increases in CRP.
Several supplements can enhance the antiin¬‚ammatory effect of a
nutrient-dense diet.
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FISH-OIL SUPPLEMENTS
Fish-oil supplements contain substantial amounts of omega-3 fats,
specifically eicosapentaenoic acid (EPA) and docosahexaenoic acid
(DHA). They reduce levels of prostaglandin E2 and other in¬‚amma-
tion-promoting compounds, resulting in lower medication require-
ments. Omega-3 fish oils, in a range of 1 to 5 grams daily, are
particularly helpful in arthritis because they inhibit aggrecanases, a
family of enzymes that break down cartilage.

GAMMA-LINOLENIC ACID (GLA)
Although GLA is an omega-6 fat, it behaves more like an antiin¬‚am-
matory omega-3 fat, and the two are synergistic. Several studies have
found that GLA, in dosages of 1.4 to 2.8 grams daily, is particularly
helpful in rheumatoid arthritis. Supplement sources include borage,
black currant, and evening primrose seed oils. The dosage is far more
important than the source.

ANTIOXIDANTS
As a general rule, antioxidants have antiin¬‚ammatory properties. Sev-
eral studies have found that vitamin E can lower IL-6 and CRP levels
by as much as 50 percent. Consistent with this antiin¬‚ammatory effect,
vitamin E can also ease symptoms of rheumatoid arthritis. Other
antioxidants, particularly ¬‚avonoids, such as Pycnogenol and quercetin,
have potent antiin¬‚ammatory properties. They work in part by reduc-
ing the activity of genes involved in in¬‚ammation, including those that
program adhesion molecules.


Osteoporosis
What Happens
Osteoporosis refers to a serious reduction in the density of bone, which
increases the risk of fractures and falls. According to the National
Osteoporosis Foundation, 10 million Americans have osteoporosis, and
18 million more have low bone mass (or low bone-mineral density).
Eighty percent of people with osteoporosis are women. Each year
osteoporosis accounts for 1.5 million fractures of the hip, wrist, verte-
brae, and other bones.
Contrary to popular opinion, bones are not completely solid.
Under a microscope they look porous, somewhat like a dry sponge. As
bone-mineral density decreases and osteoporosis develops, the natural
192 F E E D YO U R G E N E S R I G H T


openings in bone increase in size. With lower mineral density, bones
become more likely to break under stress.
Because of advertising by the dairy industry, many people believe
that calcium is the only nutrient needed for healthy bones. In truth,
your bones are living tissue, consisting of a matrix of calcium, magne-
sium, other minerals, and protein. Every day your body forms new
bone and breaks down old bone. As you get older, particularly if you
are a postmenopausal woman, you have to work a little harder to main-
tain normal bone density.

The Gene Connection
In recent years considerable research has focused on the role of vitamin
D in maintaining and increasing bone density. Without vitamin D your
body cannot put calcium to work. Yet large numbers of people carry
polymorphisms in the vitamin D receptor gene (VDR) that interfere
with the body™s use of the vitamin. (See “The Vitamin D Quandary” in
this chapter.)
Some specific VDR polymorphisms are common in people
with osteoporosis. Because these polymorphisms reduce the ef¬ciency of
vitamin D metabolism, the consequence is often similar to an outright
vitamin D deficiency. With low vitamin D activity, all vitamin D“
dependent activities, including calcium utilization, are reduced.

What You Can Do
The effect of VDR polymorphisms can be overcome with increased
production or intake of vitamin D. By spending ¬fteen minutes daily in
the sun, you can ensure that your body will make adequate amounts of
vitamin D. If you spend most of your time indoors or if you live in a
cloudy climate, consider taking 400 to 800 IU of supplemental vitamin
D each day.

CALCIUM VITAMIN D
AND
Combining calcium and vitamin D supplements can make a big differ-
ence in bone health. In a study of 389 elderly men and women, Dr. Bess
Dawson-Hughes of Tufts University reported that daily supplements of
calcium (500 mg) and vitamin D (700 IU) for three years signi¬cantly
increased bone density. People taking the supplements had half the
fractures of a group taking a placebo.
According to a 1997 report issued by the National Academy of Sci-
ences, most Americans do not consume enough calcium. In that report
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researchers noted that most people fail to obtain the recommended
amounts of calcium (1,000 mg daily for people ages twenty-¬ve to ¬fty
and 1,200 mg daily for people over age ¬fty-one). Only 10 percent of
the elderly receive adequate calcium.

MAGNESIUM
The mineral magnesium is, in importance, second only to calcium in
bone, and high calcium intake can suppress magnesium levels. In fact,
magnesium deficiency, whatever the cause, contributes to weaker
bones. In one study Austrian researchers gave magnesium supplements
to 24 men in their twenties and thirties. After a month the men bene-
¬ted from lower bone turnover, a sign of greater resistance to osteo-
porosis. A bene¬cial amount is 300 to 400 mg daily.

VITAMIN K
The body™s production of several bone-building proteins, including
osteocalcin, requires vitamin K. James Sadowski, Ph.D., and his col-
leagues at Tufts University gave 9 healthy young men and women 420
mcg of vitamin K daily. After ¬fteen days tests indicated that the sub-
jects™ bone density increased, according to an article in the American
Journal of Clinical Nutrition. Consider taking 100 to 400 mcg daily, but
discuss this supplement with your doctor if you are taking anticoagu-
lant (blood-thinning) medications.

VITAMIN B 12
Vitamin B12 stimulates the activity of two types of osteoblasts, cells
needed for bone formation. Your supplement regimen should include
100 to 500 mcg daily.

VITAMIN C
Proteins are woven into the matrix of minerals in bones, and vitamin C
is needed to make these proteins. A study of 1,892 middle-aged women
in the Seattle area found that those taking vitamin C supplements for
at least ten years had higher bone density than women who did not
take supplements. The dosage is not speci¬c but may vary from 500 to
2,000 mg daily.

DIETARY CONSIDERATIONS
Several studies have found that high intake of nonstarchy vegetables
is associated with increased bone density. In addition, mineral water
194 F E E D YO U R G E N E S R I G H T


provides substantial amounts of calcium and magnesium, and antioxi-
dants in green tea also appear to promote bone density.

WEIGHT-BEARING EXERCISES
Walking, weight lifting, and other exercises that place weight on the
bones increase bone density. Even modest levels of physical activity are
helpful.

If you have been diagnosed with osteoporosis, ask your physician to
test you for celiac disease. (See the “Celiac Disease” section in this
chapter.) Grains interfere with calcium absorption, and approximately
3 percent of people with osteoporosis have celiac disease. However,
about one-fourth of people with celiac disease have osteoporosis,
chie¬‚y because of poor nutrient absorption.


k
The Vitamin D Quandary
For years dietitians have cautioned about excessive intake of vitamin D
supplements. The body can store the vitamin, and chronic excesses are
potentially fatal, though toxicity and fatalities are extremely rare.
Today a growing concern in medicine is over whether people get
enough vitamin D. Several large studies have found that vitamin D
de¬ciencies are common, particularly among the elderly and people
with osteoporosis.
At last count, researchers have identi¬ed ¬fteen polymorphisms in
the vitamin D receptor gene (VDR). This gene programs the construc-
tion of the vitamin D receptor in cells, and the VDR is the ultimate
arbiter of how well your body uses vitamin D. When the VDR cannot
function ef¬ciently, vitamin D activity decreases throughout the body.
VDR polymorphisms are surprisingly common, and they have been
identi¬ed in people with osteoporosis, periodontal disease, type 2 dia-
betes, Addison™s disease, in¬‚ammation, psoriasis, and breast, prostate,
and colon cancers. Indeed, the relationship between low vitamin D lev-
els and cancer is so well established that there is widespread research
on synthetic forms of vitamin D as chemotherapeutic drugs for the
treatment of cancer. Low levels of vitamin D also have been found in
people with type 1 diabetes, multiple sclerosis, and congestive heart
failure, suggesting that VDR gene polymorphisms may be involved in
these diseases as well.
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Thousands of years ago, when humans spent much of their time
outdoors, VDR polymorphisms were of no serious consequence. Sun-
light initiates the conversion of cholesterol in the skin to vitamin D.
People make prodigious quantities of vitamin D when exposed to sun-
light for just a few minutes (and before they get sunburned). These
huge amounts of vitamin D saturate the VDR, enabling it to function at
optimal levels, regardless of whether a polymorphism is present.
VDR polymorphisms have become more of a health issue because
many people now spend much of their time indoors (at home and at
work), or they wear sun-blocking clothing and sunscreen while out-
doors. In addition, grain consumption reduces vitamin D absorption.
Today many of us have little regular exposure to sunlight”our avoid-
ance often compounded by fears of skin cancer”and relatively few
dietary sources of vitamin D.
The vitamin D made by your body is extraordinarily safe”no cases
of endogenous vitamin D toxicity have ever been reported. The body
regulates its own vitamin D production, shutting it off when levels are
adequate. If you don™t spend much time in the sun, consider taking 400
to 800 IU of vitamin D daily.
k
Obesity and Type 2 Diabetes
What Happens
Obesity and type 2 (adult-onset) diabetes are almost always linked.
Underlying both of these disorders is insulin resistance, reflecting
impaired glucose tolerance and the overconsumption of re¬ned carbo-
hydrates and sugars.
Here™s what happens: The starches and sugars in refined and
processed foods (such as pastas, breads, sugary soft drinks, muf¬ns,
bagels, pastries, and candy bars) are quickly digested, leading to a rapid
increase in blood-glucose levels. Elevated glucose triggers the secretion
of insulin, the hormone that lowers glucose levels by shuttling it from
the blood into cells.
For many years elevated insulin levels (an early sign of diabetes
risk) can maintain normal glucose levels. However, at a certain point
cells will start to resist (or become insensitive to) the action of insulin.
When this happens, both glucose and insulin levels remain abnormally
high, increasing the risk of elevated cholesterol and triglyceride levels,
hypertension, coronary artery disease, blindness, kidney disease, nerve
196 F E E D YO U R G E N E S R I G H T


damage, circulatory problems leading to amputation, Alzheimer™s dis-
ease, and cancer.
The health problems are not just related to high levels of glucose
and insulin. Even small increases in blood-sugar levels, well within the
normal range, can signi¬cantly boost the risk of diabetes and death
from heart disease, according to several recent studies. Furthermore,
according to Dr. David S. Ludwig of the Harvard Medical School, reg-
ularly eating high-carbohydrate and high-sugar foods creates an up-
and-down blood-sugar cycle, leading to frequent bouts of hunger and
encouraging the consumption of still more high-calorie foods.
Elevated glucose levels re¬‚ect the consumption of excessive carbo-
hydrate calories and, often, a lack of compensatory physical activity to
help burn those calories. High levels of glucose start what is essentially
a free-radical chain reaction, and these free radicals are responsible for
some of the tissue destruction associated with diabetes. However, ele-
vated insulin levels may actually be responsible for far more tissue
damage.

The Gene Connection
Some population groups, such as the Pima Indians of southern Arizona,
are especially prone to obesity and diabetes. Approximately two-thirds
of Pima Indians are obese and one-half have diabetes, suggesting a
particularly strong genetic predisposition for these diseases. However,
no single “smoking gun” gene has been consistently identi¬ed as the
cause of obesity or diabetes in any group of people.
Rather, the rapidly increasing worldwide prevalence of obesity and
diabetes re¬‚ects the abnormal juxtaposition of a modern re¬ned diet
on our ancient genes. As traditional populations around the world”for
example, Australian aborigines, black Africans, Paci¬c Islanders, and
Yemenite Jews”have adopted Westernized eating habits, their inci-
dences of obesity and diabetes have increased by up to forty times.
The risk of diabetes is lower among people of Northern European
heritage, suggesting a delayed response to a diet that promotes obesity
and diabetes. (It is possible that ten thousand years of re¬ned-grain
consumption in Europeans and the ancestors of Europeans has
selected for the survival of people with greater resistance to diabetes.)
However, in the United States alone, two-third of adults are now over-
weight or obese, and the incidence of diabetes increased by 36 percent
during the 1990s alone.According to a 2003 report from the Centers for
Disease Control and Prevention, one of every three children born in
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2000 will likely become diabetic because of poor eating habits and a
lack of exercise.
A variety of nutritional, biochemical, and genetic factors are at play
in obesity and diabetes. As people consume more re¬ned carbohy-
drates and sugars, their metabolism increasingly resembles prediabetic
patterns of blood glucose and insulin. Elevated glucose levels increase
the formation of free radicals and advanced glycation end products,
both of which damage DNA and other cell structures. Meanwhile, ele-
vated insulin levels alter normal gene behavior, increasing the number
and size of fat cells around the belly, accelerating the development of
coronary artery disease, and increasing the risk of breast cancer and
other types of cancer.
The situation in the United States has been exacerbated by a sig-
ni¬cant increase in the number of calories consumed.This trend started
about ¬fteen years ago, with “supersize” and larger “value” meals sold
at fast-food restaurants, and it is now being exported to Europe and
Asia. Food portion sizes are larger today than they were twenty years
ago. When public health authorities recommended low-fat diets
(purportedly to reduce the risk of heart disease), food companies
responded by making and marketing thousands of low-fat and no-fat
foods”but the fat was replaced with re¬ned carbohydrates and sugars.
Diets high in re¬ned carbohydrates and sugars displace more nutri-
tious foods, such as ¬sh, meat, and vegetables. As a consequence, peo-
ple consume fewer nutrient-dense foods and lower levels of the very
nutrients (such as B vitamins, alpha-lipoic acid, carnitine, and vitamin
C) needed to break down and burn carbohydrates and sugars for
energy. Indeed, a study in the February 12, 2004, issue of the New
England Journal of Medicine found that defects in mitochondrial activ-
ity lead to the accumulation of fat in muscle and greater insulin resist-
ance in patients with type 2 diabetes.

What You Can Do
In most people obesity and diabetes are nutritional diseases, and they are
best treated nutritionally. Your ¬rst step should be to adopt a nutrient-
dense diet, consisting of protein and ¬ber-rich vegetables (see chapter 7).
Protein and ¬ber help stabilize and lower both blood-glucose and insulin
levels. One immediate bene¬t of such eating habits will be a reduction in
hunger pangs, leading to less snacking and overeating and a loss of
weight.You may not eliminate a tendency toward obesity or diabetes, but
such eating habits will certainly help you avoid these two diseases.
198 F E E D YO U R G E N E S R I G H T


Several supplements have been found helpful in reducing glucose
levels and enhancing insulin function. It is far better for your body to
use less insulin but to use it more ef¬ciently.

CHROMIUM
Chromium, an essential mineral, is needed for the proper functioning
of insulin. Studies by Dr. Malcolm N. McLeod, a psychiatrist at the
University of North Carolina School of Medicine, found that chromium
picolinate supplements (averaging 400 mcg daily) relieved depression,
reduced hunger and appetite, and, in some patients, led to signi¬cant
weight loss. A separate study by U.S. and Chinese researchers found
that 1,000 mcg of chromium picolinate daily reduced glucose and
insulin levels to almost normal after four months.

SILYMARIN
This antioxidant extract of milk thistle (Silybum marianum), silymarin
is widely used to enhance the function of the liver, which works in tan-
dem with the pancreas to regulate glucose levels. In a twelve-month
clinical study, 600 mg daily of silymarin reduced glucose in diabetic
patients by 9.5 to 15 percent. The patients also bene¬ted from lower
levels of sugar in the urine, less glycated hemoglobin, and lower insulin
requirements.

ALPHA-LIPOIC ACID
Like silymarin, alpha-lipoic acid also improves insulin function and
lowers blood-sugar levels. It is widely used in Germany to treat diabetic
symptoms, including nerve damage. Alpha-lipoic acid helps the body
break down and burn glucose for energy, and as an antioxidant it pro-
tects against diabetic complications.
In a series of animal experiments described in the journal Nature
Medicine in 2004, researchers reported that supplemental alpha-lipoic
acid reduced appetite and led to both weight and fat loss. According
to the researches, alpha-lipoic acid worked by reducing levels of
the enzyme AMP-activated protein kinase (AMPK). AMPK levels
increase when cell reserves of glucose and fat decrease, and it plays a
key role in stimulating hunger. The therapeutic dose of alpha-lipoic
acid is 200 mg three times daily.

CINNAMON
Richard A. Anderson, Ph.D., and his colleagues recently treated dia-
betic subjects with 1, 3, or 6 grams of cinnamon or a placebo daily. (One
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gram of cinnamon is about one-quarter teaspoon of the ground herb.)
Overall, people receiving cinnamon bene¬ted from 18 to 29 percent
decreases in fasting glucose levels, 7 to 27 percent declines in choles-
terol levels, and 23 to 30 percent reductions in triglyceride levels. In
general, larger amounts of cinnamon had greater bene¬ts.

APPLE CIDER VINEGAR
Carol S. Johnston, Ph.D., of Arizona State University, asked three groups
of subjects to drink 20 grams of apple cider vinegar before consuming a
high-carbohydrate breakfast containing 87 carbohydrate grams from a
bagel, butter, and orange juice. The subjects included 11 people with
insulin resistance, 10 with type 2 diabetes, and 8 healthy controls. A week
later all the subjects were given a placebo drink followed by the same
high-carbohydrate breakfast. All of them benefited from smaller
increases in glucose and insulin after consuming the apple cider vinegar.


Parkinson™s Disease
What Happens
Parkinson™s disease is the second most common neurodegenerative
disorder after Alzheimer™s disease. It affects an estimated 1 million
Americans, and about 60,000 new cases are diagnosed each year.
Although Parkinson™s disease is often diagnosed in people in their for-
ties, the average age of onset is about sixty years.
People in the advanced stages of the disease have a haunting and
unsettling look: their torso remains unnaturally rigid, while tremors
uncontrollably shake the arms, hands, legs, and jaw. In addition, balance
and coordination are impaired, so people with the disease shuf¬‚e about
slowly and unsteadily.

The Gene Connection
Although several inherited genes are involved in rare forms of Parkin-
son™s disease, no clear genetic predisposition has been identi¬ed in the
more common forms of the disease. Twenty percent of patients with
Parkinson™s disease have a close relative with the disease, suggesting a
genetic component. However, 80 percent of cases have no obvious
inherited risk.
The disease is better understood in biochemical terms. It is charac-

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