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"Functional foods," "nutraceuticals,"
"designer foods" and "medicinal foods" are terms that describe
foods, and key ingredients isolated from foods, that have non-nutritive
or tertiary functional properties. Researchers, healthcare practitioners,
laypersons, and the popular media use these words interchangeably.
The purpose of this article is to review the medicinal properties inherent
in food sources of folate, a known anti-colon cancer nutrient, and
to discover other nutritive factors (such as glutamine, glucosinolates,
and fiber) within those same foods that support colon health and maintain
intestinal integrity.
Enhancing the Effects of Folate with Whole Foods that Prevent Colon
Cancer and Maintain Intestinal Integrity
There is substantial evidence to
indicate that sufficient levels of folate in the daily diet can prevent
or at least reduce the incidence
and onset of colorectal cancer. A folate deficiency can cause and promote
DNA mutations by increasing DNA's susceptibility to damage by
carcinogenic compounds, while sufficient levels of folate in the body
can reduce the risk of clinically evident colon cancer.1,2 In
1998, a follow up of the famous Nurses' Health Study completed on 88,756
female nurses found that 15 years of high folate intake (> 400 mcg/day)
was associated with a 75% reduction in risk for colon cancer.3 This
was a prospective cohort study with a very large sample size, and the
resultant data was adjusted for alcohol intake, age, physical activity,
red meat consumption, fiber intake, smoking history, family history
and even aspirin use.
Another cohort study investigated the relative risk for colon cancer in men,
based on folate intake. The National Health and Nutrition Examination Survey
(NHANES) Follow-up Study (NHEFS)4 found that the relative risk of colon cancer
for participants in the study was 60% less in those men that ingested over
239 mcg of folate in their diet per day as compared to those men that took
in less than 103.3 mcg of folate per day.
Whole food sources of folate range from chicken liver (770 mcg per 3.5 oz)
to cooked lentils (180 mcg per 1/2 cup), Brussels sprouts (47 mcg per 1/2 cup)
and broccoli (39 mcg per 1/2 cup). Interestingly, key vegetable sources of
folate, such as cruciferous vegetables and beets, contain additional compounds
specific for reducing colon cancer risk and supporting intestinal health, such
as glutamine, glucosinolates, and fiber.
Cruciferous Vegetables and Colon Cancer
In addition to the folate-related actions that cruciferous vegetables (e.g.,
kale, Brussels sprouts, cabbage and broccoli) have on preventing or reducing
the risk of colorectal cancer, these vegetables also contain glucosinolate
compounds that cause a coordinated metabolic induction of many of the Phase
II liver detoxification enzymes. These enzymes detoxify carcinogenic compounds
from the body, thus reducing the susceptibility of colon cells to DNA damage.
Glutathione transferases, NAD(P)H, quinone oxidoreductase, glucuronosyltransferase,
and epoxide hydrolase are all Phase II enzymes that inactivate environmental
carcinogens known to increase one's risk of developing colon cancer.
Phase II Detoxification Enzyme Inducers that Reduce the Risk of Developing
Colon Cancer
Phase II enzymes inactivate carcinogens in one of two ways: either through
the destruction of the reactive centers of the compounds, or, more often, by
conjugation with endogenous ligands, thereby counteracting the toxic properties
associated with the carcinogen, and quickening their elimination from the body.
Cruciferous vegetables contain water-soluble secondary metabolites referred
to as glucosinolate compounds.
Glucosinolates found in cruciferous vegetables are converted by endogenous
enzymes into isothiocyanates when they are chewed, crushed in the presence
of water, or otherwise injured. This conversion is a natural defense response
to predatory and other destructive influences. The tissue damage more specifically
results in the release of the endogenous enzyme myrosinase, or thioglucosidase,
which cleaves the glucoside bond. This results in an unstable intermediate
which rearranges to release sulfate, isothiocyanates and other products.
The isothiocyanates are the principal inducers of Phase II liver detoxification
enzymes. Sulforaphane and sinigrin are two isothiocyanates that protect against,
and oftentimes reduce, the severity of colon cancer.5 Sulforaphane supports
the enzymatic activity that takes place in Phase I liver detoxification and
assists the liver in carrying out the Phase II conjugation pathways. Sinigrin
complements the activity of sulforaphane by also stimulating the Phase II detoxification
system. In addition to supporting the liver detoxification system, sinigrin
stimulates apoptosis, a process that naturally causes a damaged cell to fragment
into membrane-bound particles that are then eliminated by phagocytosis.6 Organosulfur
compounds such as dithiolethiones that are found in cruciferous vegetables
are also considered putative detoxifying agents via their effect on Phase II
enzymes.7,8
Inducing Detoxification of Environmental Mutagens that Lead to Colon
Cancer
Isothiocyanates have specifically been shown to induce the detoxification of
environmental mutagens that can lead to colon cancer.9
Interestingly, 50% of people completely lack the glutathione-S-transferase
M1 (GSTM1) enzyme due to a homozygous gene deletion. This enzyme is responsible
for the rapid conjugation of isothiocyanates to glutathione for excretion (Phase
II). Lin et al.10 hypothesized that people with this mutation would maintain
higher levels of isothiocyanates in the body due to decreased excretion and
should show a lower incidence of colorectal adenomas, the precursors of colorectal
cancer, if isothiocyanates are indeed anticarcinogenic. The researchers found
that broccoli (39 mcg of folate per 1/2 cup) and kale were significantly associated
with a lower prevalence of colorectal carcinomas in a sample of nearly a thousand
people (459 adenoma cases and 507 controls sampled from patients undergoing
cancer sigmoidoscopy screening in southern California). The presence of the
GSTM1 null genotype alone did not significantly correlate with the occurrence
of colorectal carcinoma. However, the GSTM1 null genotype did correlate with
a significant reduction of incidence of colorectal carcinoma when it was covaried
with broccoli and total cruciferous vegetable consumption (p=0.001 and p=0.02,
respectively). The lowest incidence of colorectal carcinoma occurred in GSTM1
null individuals in the highest quartile of broccoli consumption, supporting
the hypothesis that isothiocyanates in crucifers may be excreted more slowly
in urine in GSTM1 individuals.
In addition to glucosinolate compounds, some crucifers contain significant
levels of the amino acid glutamine, also important in supporting the detoxification
system and maintaining optimal intestinal health.
Glutamine and Intestinal Health
Glutamine: Another Compound Found in Vegetable Sources of Folate (Cabbage
and Beets) that Supports Intestinal Health
Glutamine is the most abundant amino acid in the blood stream (30-35%
of amino acid nitrogen in plasma) and fills a number of detoxification-associated
biochemical
needs in the body.11 It is a conditionally-essential amino acid, in that
the human body produces it endogenously. Deficiencies are prevalent
however, primarily
because of impaired detoxification mechanisms, cancer, burns, trauma, chronic
protein catabolism and excessive exercise.12,13
This amino acid is the main metabolic fuel for enterocytes of the small intestine,
lymphocytes, macrophages, and fibroblasts and plays a major role in the first
line of immune defense in the intestine as well as in the body as a whole.
Interestingly, this supportive nutrient is found in particularly high concentrations
in two vegetable sources recognized for their detoxifying properties and
folate content: cabbage and beets.14-18
Research suggests that glutamine is essential to the health and maintenance
of the intestinal tract, a vital organ of detoxification.19,20 In fact, the
intestine is the greatest user of glutamine in the body. The intestinal enterocytes
absorb glutamine from the lumen of the gut and the bloodstream. The intestinal
cell mitochondria then convert glutamine to glutamate, and then to alpha-ketoglutarate,
which is used in the Krebs cycle for ATP production.
Studies have shown that the level of stored glutamine drops significantly
in humans following surgery, trauma, or burns, as well as during sepsis.21-23
It is well recognized that such conditions cause a state of imbalance of
beneficial
organisms in the intestinal tract.
Its deficiency has been implicated in immune dysfunction, a condition also
associated with impaired detoxification mechanisms, because it serves as
a main precursor of nucleotide synthesis and also as an energy source for
rapidly
dividing cells, such as immune cells following an immune threat.24-26
Prevention of Microbial Translocation
Glutamine's positive effect on the GI tract appears to be due to its
use as a food source by both intestinal immune cells (lymphocyte-rich Peyer's
patches) and mucosal cells. Intestinal epithelial cells contain very low levels
of glutamine synthetase and hence are largely dependent on pre-formed glutamine,
either from the diet or from the blood. If glutamine is lacking in the diet,
or if a person is being fed parenterally due to illness, intestinal cells will
take glutamine from the blood stream at the expense of muscle tissue, thus
depleting the body's stores.27 When levels of glutamine drop, intestinal
epithelial cells and lymphocytes begin to lose function, compromising the integrity
of the epithelium and leaving the intestine vulnerable to microbial translocation
(passage of bacteria or toxins into the bloodstream via the intestinal wall).28-33
Several factors can disrupt intestinal permeability leading to increased microbial
translocation, including:
• Impaired Detoxification Pathways
• Trauma
• Infection
• Starvation
• Chemotherapy
Bacteria, fungi, and other toxins can translocate across the weakened mucosal
barrier into the bloodstream, where they react with the reticuloendothelial
system, stimulating production of cytokines via the hypothalamic-pituitary-adrenal
axis.34 Cortisol is subsequently released from the adrenals, which increases
glutaminase activity in intestinal enterocytes, thereby increasing breakdown
of glutamine in the small intestine. This results in a progressive depletion
of glutamine and glutathione (which contains glutamine) from skeletal muscle,
leading to oxidative muscle tissue damage.
Additionally, glutamine increases intestinal glutathione synthetase activity,35
improving the antioxidant capacity of the gut and increasing the mitogenic
response to immune threats.36 Gut-associated lymphoid tissue (GALT) requires
glutamine for optimal function. GALT comprises the Peyer's patches and
lymphoid follicles scattered throughout the intestinal mucosa. It is in this
tissue that B and T immune cells are primed against intestinal antigens, thus
forming a "frontline" defense of memory cells that can be seeded
in distant mucosal effector sites. Maintenance of immune function and a healthy
intestinal tract is vital to supporting one's ability to eliminate environmental
toxins from the body.
Mechanisms of Action of Cabbage: A Food Source of Glutamine with Known
Chemopreventive and Immunoprotective Properties
In addition to its glutamine (and folate and glucosinolate) content, other
factors within cabbage contribute to its inherent immunoprotective and chemopreventive
properties. Cabbage stimulates the production of tumor necrosis factor a (TNF)
and interleukin-1 (IL-1), important players in antitumorial, antiviral, immunoregulatory,
and inflammatory responses.37 Further, cabbage contains glucosinolates and
their breakdown products that alter the induction of glutathione S-transferase
(GST), NADPH, and Quinone oxidoreductase (NQO),38 thereby supporting detoxification
of colon cancer-causing agents in the body.
The GST family of detoxification enzymes are responsible for conjugating electrophilic
compounds with glutathione, creating a more water-soluble, and usually non-cytotoxic
compound to be excreted. The flavoprotein NQO functions as a catalyst for the
reduction of a wide range of quinones, quinone imines, and azo dyes via a two-electron
transfer. Researchers speculate that the protective action of NQO is a result
of its successful competition with single-electron reduction reactions and
the inhibition of oxidative metabolic intermediates.39This augmentation in
free radical production reduces the total burden placed on the immune system.40
Some of the known medicinal constituents in cabbage include 4-Me-glucobrassicin,
progoitrin, 4-OH-glucobrassicin, R-goitrin, sinigrin, flavonoids, glucoiberin,
gluconapin, thiocyanates, glutamine, isothiocyanates, phenolic compounds, and
indole-3-carbinol.41-43
Maintenance of intestinal integrity and immune function
Komatsu et al.44 administered cabbage juice to normal and hepatome-bearing
rats. In this study, cabbage juice stimulated tumor necrosis factor a (TNFa)
and interleukin-1 (IL-1) in the normal rats but failed to do so in the hepatome-bearing
rats, whose levels of these enzymes were already elevated. The cabbage demonstrated
immune stimulatory properties which the authors speculate was due to some "unknown" effective
component that can be absorbed from the GI tract to stimulate production
of TNFa and IL-1. This component may be glutamine, although other functional
constituents within cabbage cannot be ruled out. TNFa and IL-1 are the primary
cytokines produced by activated macrophages. Additionally TNFa plays an important
role in antitumor, antiviral, immunoregulatory, and inflammatory responses.
Administering vegetables that contain glutamine, in addition to other known
tertiary compounds (such as folate and glucosinolates), would likely offer
a greater clinical effect on colon/intestinal health than the sum of the components
in isolate form.45 A further example of a glutamine-rich food that contains
complementary compounds such as folate and fiber that support colon health
is beta vulgaris, commonly referred to as beet root.
Beta vulgaris (Beet Root) and Colon Health
Beet root represents another vegetable that contains multiple constituents
that function to support intestinal health and prevent colon cancer via at
least several known mechanisms. A sampling of the known medicinal constituents
within beet include sugars [e.g., folate, saccharose, oligosaccharides, and
polysaccharides (galactans, arabans, pectin)], fruit acids (e.g., L(-)-malic,
D(+)-tartaric, oxaluric, adipic, citric, glycolic, and glutaric acids), amino
acids (e.g., asparagine, glutamine), betaine (trimethylglycine) and triterpene
saponins.46
In addition to beet root's actions in supporting colon/intestinal health
due to its folate and glutamine content, animal studies have shown dietary
beet root fiber to reduce serum and liver lipids,47-49 which are known risk
factors in colon cancer.50
Beet and lipid metabolism
Sugar beet fiber fed to rats as 30% of a low fat diet for three weeks significantly
decreased ileal apolipoprotein B mRNA expression that is responsible for
LDL cholesterol synthesis.51 As a possible consequence, fecal bile salt and
cholesterol excretions were elevated. Beet fiber also significantly increased
hepatic LDL receptor mRNA and lowered serum total and LDL cholesterol levels
relative to cellulose and mushroom fiber (chitin) in rats.52 The beet's
demonstrated lipid lowering effect may be a result of the food's ability
to increase the uptake of LDL cholesterol by the liver.
Protective properties of beet on the colon
Bobek et al.53 examined the effect of red beet
fiber on the development of alimentary hypercholesterolemia and dimethylhydrazine-induced
carcinogenesis
in the rat colon. The researchers showed that 15% red beet fiber in a hypercholesterolemic
diet (0.3% dietary cholesterol) reduced serum cholesterol and triacylglycerol
levels by 30% and 40%, respectively, and increased the fraction of HDL cholesterol.
Of particular interest to researchers is the significant decrease in aortic
cholesterol (nearly 30%) (Table 1, below).
Red beet fiber caused a pronounced increase in the activities of superoxide
dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase
enzymes in colon, liver, and erythrocytes, supporting the hypothesis that oxidation
pathways contribute to the disease state (data not shown), and illustrating
that beet fiber likely promotes Phase II detoxification function in the intestine,
blood, and liver. In addition, dietary red beet fiber reduced the incidence
of precancerous lesions in the rat colon. Other animal studies support the
finding that dietary beet fiber dose-dependently decreases serum and liver
cholesterol levels and offers some protection against colon cancer.54,55
Table 1
Lipids in serum, lipoproteins,
and organs of rats fed a hypercholesterolemic diet
with 5% cellulose,
15% cellulose, or 15% red beet fiber.
Parameter
N
Body weight (g)
Cholesterol
Serum (mmol/L)
VLDL (mmol/L)
%VLDL*
LDL (mmol/L)
%LDL*
HDL (mmol/L)
%HDL*
Liver (mmol/kg)
Heart (mmol/kg)
Aorta (mmol/kg)
Triacylglycerols
Serum (mmoi/L)
Liver (mmol/L)
Heart (mmol/kg)
|
Diet 5% Cellulose
11
450±16
9.93±0.22
1.86±0.13
19.2±1.1
4.72±0.43
48.5±1.9
3.14±0.24
32.3±1.1
511±7
10.06±0.66
7.46±0.33
0.76±0.03
48.6±4.2
1.54±0.11
|
15% Cellulose
12
455±16
9.19±0.47
1.61±0.11
18.4±1.1
3.93±0.37
45.1±1.6
3.19±0.25
36.5±1.3
496±13
9.78±0.66
7.23±0.37
0.67±0.05
38.1±5.82
1.17±0.15
|
15% Red beet fiber
11
471±17
6.82±0.53b,C
0.69±0.07c,C
10.6±0.9c,C
2.79±0.36B
42.7±2.0
3.05±0.43
46.7±1.9C
523±22
8.67±0.49
5.54±0.34b,B
0.44±0.03c,C
45.1±6.9
1.26±0.18
|
* Fraction of total serum cholesterol
Statistically significant against 5% cellulose diet:
Ap<0.05 Bp<0.01 Cp<0.00l
Statistically significant against 15% cellulose diet:
ap<0.05 bp<0.01 cp<0.00l
Final Thought
Given the complexity and overlapping roles of the intestinal tract, the immune
system and the human detoxification system, it is unlikely that any single
nutrient, such as folate, is wholly responsible for the effects that foods
such as broccoli, cabbage and beets impart on the body's ability to
stave off colon cancer and maintain intestinal health.
Correspondence
Gina L.
Nick, PhD, ND
PO Box 627 · Brookfield, Wisconsin
53008 USA
Phone: 866.587.4622 Fax: 262.569.9571 E-mail: drgina@ltponline.com
http://www.ltponline.com
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