Anti-kanker dieet
Af en toe vind ik kleine juweeltjes op
het net. Het onderstaande artikel is helaas in het Engels maar misschien dat iemand wil
helpen dit artikel voor andere lezers te vertalen. Ik ben te druk met het zoeken naar
nuttige info dus alle hulp is welkom.
In de korte versie (abstract) staat
eigenlijk alles samengevat en wordt wederom de rol van lijnzaadolie genoemd (flaxseed),
deze olie komt ook terug in het antikanker dieet van Anna Budwig uit de jaren vijftig
(Budwig papje). Ook worden de broccoli kiemen (liggen nu ook hier in de supermarkt) en rol
van selenium, b12, vitamine d, folium zuur, lycopeen (tomaten puree), vitamine C en
chlorophyl (groene groentes, algen) genoemd.
Een echte aanrader!
Ron
Korte samenvatting Mike Donkers:
Naar schatting 30 tot 40 % van de
bestaande kankers kunnen voorkomen worden door alleen al maatregelen te nemen op het
gebied van dieet en levensstijl.
Voedingsarme stoffen zoals
geconcentreerde suikers en verfijnde meelprodukten, die mede veroorzakers zijn van een
slecht functionerende glucose stofwisseling (dat op zijn beurt weer leid tot diabetes)
lage vezelinname, consumptie van rood vlees en een slechte balans van Omega 3 en 6
vetzuren dragen allen bij aan het bestaan van een overmatig risico op de ontwikkeling van
kankers.
De inname van vlaszaad en met name het
lijnzaad gedeelte evenals overvloedige hoeveelheden groente en fruit zullen het risico op
het ontwikkelen van kanker verlagen.
Vooral Allium en kruisbloemige groenten
zijn heilzaam waarbij broccoli relatief gezien het meeste Sulforophane bevat.
Beschermende elementen in een dieet ter
preventie van kanker zijn onder andere selenium, foliumzuur, vitamine B-12, vitamine D,
chlorofyl en anti-oxidanten zoals de carotenen (A-caroteen, B-caroteen, lycopene, luteine,
cryptoxanthine).
Ascorbinezuur heeft weinig effect als het
oraal ingenomen wordt maar zou intravenously (geinjecteerd?) wel behulpzaam kunnen zijn.
Aanvullende orale inname van digestieve enzymen en probiotics heeft ook nut als dieet
onderdeel tegen de ontwikkeling van kanker.
Een dieet samengesteld volgens deze
richtlijnen leid waarschijnlijk tot een afname van minimaal 60 tot 70% op het ontwikkelen
van borst, darm en prostaatkankers en zelfs tot een 40 tot 50% afname op het ontwikkelen
van longkanker, dit tezamen met gelijkwaardige afnames van kansen voor het ontwikkelen van
kanker op andere plekken in het lichaam.
Een dergelijk dieet zou kankers kunnen
voorkomen en zou het herstel na een kanker kunnen bevorderen.
Recensie achtergrond
Het veld van onderzoek over de rol van
voeding in het kanker proces is heel breed. Naarmate het onderzoek vordert wordt ook
steeds duidelijker dat voeding bij de ontwikkeling van kankers een grote rol speelt.
Door het Amerikaans Instituut voor
Kankeronderzoek en het Wereld Kanker Onderzoeksfonds wordt geschat dat 30 a 40 % van alle
kankers door toepasselijke dieten, fysieke beweging en het behoud van van normaal
lichaamsgewicht voorkomen kunnen worden. Waarschijnlijk is dit percentage nog hoger bij
enkele individuele kankers.
Tot op heden is het onderzoek naar kanker
geïsoleerd van aard geweest.
Er is dan bijvoorbeeld één type voedsel of voedingstof bestudeerd op zijn invloed op de
groei of afname van een tumor of een ander eindpunt van een kanker maar slechts in een
bepaald deel van het lichaam.
Voor het bekijken van details van de ziekte mechanismen zijn dit zeer hulpzame studies, ze
slagen er echter niet in om inzicht te verkrijgen in hoe een kanker nou door middel van
dieetmaatregelen te voorkomen is.
Ze laten ook weinig los over wat men moet
eten wanneer kanker geconstateerd is en wanneer men een dieet wil volgen wat gunstig is
voor het herstel van de ziekte. Deze ¨nieuwe kijk op de situatie¨ zal zich richten op
die onderdelen van het dieet waarvan aangetoond is dat ze een groei van het kanker risico
veroorzaken.
Daarna zal de focus gelegd worden op de
dieetmaatregelen die het kanker risico verkleinen. Ter afsluiting zullen er een aantal
studies betreffende het gehele dieet aangehaald worden zodat er een beter beeld ontstaat
hoe met behulp van deze afzonderlijke onderdelen tezamen het kanker risico verkleind kan
gaan worden.
Overconsumptie van energie (calorieen)
Een van de hoofdrisico factoren voor de
ontwikkeling van kanker is de consumptie van te veel voedsel. En wel vanwege (1) het
bijkomende risico op het krijgen van ziektes door zwaarlijvigheid en (2) het feit dat het
consumeren van weinig voedsel een beschermend effect heeft.
Zwaarlijvigheid heeft in Amerika
epidemische vormen aangenomen.
64% van de volwassen bevolking heeft overgewicht of is zwaarlijvig (2) en één op de
vijftig inwoners is momenteel ernstig zwaarlijvig (BMI >40kg/m2) (3) Mokdat et al (4)
vond uit dat de combinatie van een slecht eetpatroon en te weinig beweging de op één na
belangrijkste doodsoorzaak is (400.000 doden per jaar in de VS) en dat deze combinatie
waarschijnlijk tabak gaat aflossen als doodsoorzaak nummer één.
Nutrition and cancer: A
review of the evidence for an anti-cancer diet
Abstract
It has been estimated that
30–40 percent of all cancers can be prevented by lifestyle and dietary measures
alone. Obesity, nutrient sparse foods such as concentrated sugars and refined flour
products that contribute to impaired glucose metabolism (which leads to diabetes), low
fiber intake, consumption of red meat, and imbalance of omega 3 and omega 6 fats all
contribute to excess cancer risk. Intake of flax seed, especially its lignan fraction, and
abundant portions of fruits and vegetables will lower cancer risk. Allium and cruciferous
vegetables are especially beneficial, with broccoli sprouts being the densest source of
sulforophane. Protective elements in a cancer prevention diet include selenium, folic
acid, vitamin B-12, vitamin D, chlorophyll, and antioxidants such as the carotenoids (a-carotene, ß-carotene, lycopene,
lutein, cryptoxanthin). Ascorbic acid has limited benefits orally, but could be very
beneficial intravenously. Supplementary use of oral digestive enzymes and probiotics also
has merit as anticancer dietary measures. When a diet is compiled according to the
guidelines here it is likely that there would be at least a 60–70 percent decrease in
breast, colorectal, and prostate cancers, and even a 40–50 percent decrease in lung
cancer, along with similar reductions in cancers at other sites. Such a diet would be
conducive to preventing cancer and would favor recovery from cancer as well.
Review
Background
The field of investigation of the
role of nutrition in the cancer process is very broad. It is becoming clearer as research
continues that nutrition plays a major role in cancer. It has been estimated by the
American Institute for Cancer Research and the World Cancer Research Fund that 30–40
percent of all cancers can be prevented by appropriate diets, physical activity, and
maintenance of appropriate body weight [1]. It is
likely to be higher than this for some individual cancers.
Most of the research on nutrition
and cancer has been reductionist; that is, a particular food or a nutrient has been
studied in relation to its impact on tumor formation/regression or some other end point of
cancer at a particular site in the body. These studies are very helpful in seeing the
details of the mechanisms of disease. However, they do not help give an overall picture of
how to prevent cancer on a dietary level. Even less, they tell little of how to eat when a
person already has a cancer and would like to eat a diet that is favorable to their
recovery.
This review will focus on those
dietary factors which has been shown to be contribute to increased risk of cancer and then
on those additional protective dietary factors which reduce cancer risk. Finally, some
whole-diet studies will be mentioned which give a more complete picture of how these
individual factors work together to reduce cancer risk.
Over Consumption
of Energy (Calories)
Eating too much food is one of
the main risk factors for cancer. This can be shown two ways: (1) by the additional risks
of malignancies caused by obesity, and (2) by the protective effect of eating less food.
Obesity has reached epidemic
proportions in the United States. Sixty-four percent of the adult population is overweight
or obese [2]. About 1 in 50 are now severely
obese (BMI > 40 kg/m2) [3]. Mokdad et al [4] found that poor diet and physical inactivity was
the second leading cause of death (400,000 per year in the USA), and would likely overtake
tobacco as the leading cause of death.
It was estimated in a recent
study, from a prospective cancer prevention cohort, that overweight and obesity accounted
for 14 percent of all cancer deaths in men and 20 percent of those in women [5]. Significant positive associations were found
between obesity and higher death rates for the following cancers: esophagus, colon and
rectum, liver, gallbladder, pancreas, kidney, stomach (in men), prostate, breast, uterus,
cervix, and ovary [5]. The authors estimated that
over 90,000 cancer deaths per year could be avoided if the adult population all maintained
a normal weight (BMI < 25.0) [5]. Clearly,
obesity is a major risk factor for cancer.
On the other side, careful menu
planning brings about an approach entitled CRON-Calorie Restriction with Optimal
Nutrition. The basic idea is to eat a reduced amount of food (about 70–80 percent of
the amount required to maintain "normal" body weight) while still consuming all
of the necessary amounts of vitamins, minerals, and other necessary nutrients. The only
restriction is the total amount of energy (calories) that is consumed. While being
difficult to practice, this approach has a lot of scientific merit for being able to
extend average life spans of many species of animals including rats, mice, fish, and
possibly primates (currently being tested). Along with this life span extension is a
reduction in chronic diseases that are common to mankind, reviewed in Hursting et al [6]. A recent meta-analysis of 14 experimental
studies found that energy restriction resulted in a 55% reduction in spontaneous tumors in
laboratory mice [7]. Calorie restriction
inhibited induced mammary tumors in mice [8] and
suppressed implanted tumor growth and prolonged survival in energy restricted mice [9]. Among Swedish women who had been hospitalized
for anorexia nervosa (definitely lower caloric intake, but not adequate nutrition) prior
to age 40, there was a 23% lower incidence of breast cancer for nulliparous women and a
76% lower incidence for parous women [10]. So,
too many calories is definitely counter-productive, and slightly less than normal is very
advantageous.
Glucose
Metabolism
Refined sugar is a high energy,
low nutrient food – junk food. "Unrefined" sugar (honey, evaporated cane
juice, etc) is also very concentrated and is likely to contribute to the same problems as
refined sugar. Refined wheat flour products are lacking the wheat germ and bran, so they
have 78 percent less fiber, an average of 74 percent less of the B vitamins and vitamin E,
and 69 percent less of the minerals (USDA Food database, data not shown). Concentrated
sugars and refined flour products make up a large portion of the carbohydrate intake in
the average American diet. One way to measure the impact of these foods on the body is
through the glycemic index.
The glycemic index is an
indication of the blood sugar response of the body to a standardized amount of
carbohydrate in a food. The glycemic load takes into account the amount of food eaten. An
international table of the glycemic index and glycemic load of a wide variety of foods has
been published [11].
Case-control studies and
prospective population studies have tested the hypothesis that there is an association
between a diet with a high glycemic load and cancer. The case control studies have found
consistent increased risk of a high glycemic load with gastric [12], upper aero digestive tract [13],
endometrial [14], ovarian [15], colon or colorectal cancers [16,17]. The prospective studies' results have been
mixed. Some studies showed increased risk of cancer in the whole cohort with high glycemic
load [18-20];
some studies found only increased risk among subgroups such as sedentary, overweight
subjects [21-24]; other studies concluded that there was no
increased risk for any of their cohort [25-28]. Even though there
were no associations between glycemic load and colorectal, breast, or pancreatic cancer in
the Nurses' Health Study there was still a strong link between diabetes and colorectal
cancer [29].
Perhaps the dietary glycemic load
is not consistently related to glucose disposal and insulin metabolism due to individual's
different responses to the same glycemic load. Glycated hemoglobin (HbA1c) is a
time-integrated measurement of glucose control, and indirectly, of insulin levels.
Increased risk in colorectal cancer was seen in the EPIC-Norfolk study with increasing HbA1c;
subjects with known diabetes had a three-fold increased risk of colorectal cancer [30]. In a study of a cohort in Washington county,
Maryland, increased risk of colorectal cancer was seen in subjects with elevated HbA1c,
BMI > 30 kg/m2, or who used medications to control diabetes [31]. However, glycated hemoglobin was not found to
be associated with increased risk of colorectal cancer in a small nested case-control
study within the Nurses' Health Study [32].
Elevated fasting glucose, fasting insulin, 2 hour levels of glucose and insulin after an
oral glucose challenge, and larger waist circumference were associated with a higher risk
of colorectal cancer [33]. In multiple studies
diabetes has been linked with increased risk of colorectal cancer [34-37],
endometrial cancer [38], and pancreatic cancer [35,39].
It is clear that severe dysregulation of glucose metabolism is a risk factor for cancer.
Foods which contribute to hyperinsulinemia, such as refined sugar, foods containing
refined sugar, and refined flour products should be avoided and eliminated from a cancer
protective diet.
Low Fiber
Unrefined plant foods typically
have an abundance of fiber. Dairy products, eggs, and meat all have this in common –
they contain no fiber. Refined grain products also have most of the dietary fiber removed
from them. So, a diet high in animal products and refined grains (a typical diet in the
USA) is low in fiber. In prospective health studies low fiber was not found to be a risk
for breast cancer [25]. It is possible that
fiber measurements are just a surrogate measure for unrefined plant food intake. Slattery
et al [40] found an inverse correlation between
vegetable, fruit and whole grain intake plant food intake and rectal cancer, while refined
grains were associated with increased risk of rectal cancer. A threshold of about 5 daily
servings of vegetables was needed to reduce cancer risk and the effect was stronger among
older subjects [40]. Many other nutrients are
co-variants with fiber, including folic acid, which is covered in detail below.
Red Meat
Red meat has been implicated in
colon and rectal cancer. A Medline search in February 2003 uncovered 26 reports of human
studies investigating the link between diet and colon or colorectal cancer. Of the 26
reports, 21 of them reported a significant positive relationship between red meat and
colon or colorectal cancer [17,41-64]. A recent meta-analysis also found red meat, and processed meat, to
be significantly associated with colorectal cancer [65].
Meat, and the heterocyclic amines formed in cooking, have been correlated to breast cancer
in a case-control study in Uruguay as well [66].
Omega 3:6 Ratio
Imbalance
Omega 3 fats (alpha-linolenic
acid, EPA, DHA) have been shown in animal studies to be protect from cancer, while omega 6
fats (linoleic acid, arachidonic acid) have been found to be cancer promoting fats. Now
there have been several studies that have tested this hypothesis in relation to breast
cancer, summarized in Table 1. Except for the study by London et al [67], all of these studies found an association
between a higher ratio of N-3 to N-6 fats and reduced risk of breast cancer. Long chain
N-3 and N-6 fats have a different effect on the breast tumor suppressor genes BRCA1 and
BRCA2. Treatment of breast cell cultures with N-3 fats (EPA or DHA) results in increased
expression of these genes while arachadonic acid had no effect [68]. Flax seed oil and DHA (from an algae source) both can be used to
increase the intake of N-3 fat, with DHA being a more efficient, sure source.
Flax seed
Flax seed provides all of the
nutrients from this small brown or golden hard-coated seed. It is an excellent source of
dietary fiber, omega 3 fat (as alpha-linolenic acid), and lignans. The lignans in flax
seed are metabolized in the digestive tract to enterodiol and enterolactone, which have
estrogenic activity. In fact, flax seed is a more potent source of phytoestrogens than soy
products, as flax seed intake caused a bigger change in the excretion of 2-hydroxyestrone
compared to soy protein [69].
Ground flax seeds have been
studied for its effect on cancer, including several excellent studies by Lilian Thompson's
research group at the University of Toronto. In one study the flax seed, its lignan
fraction, or the oil were added to the diet of mice who had previously been administered a
chemical carcinogen to induce cancer. All three treatments reduced the established tumor
load; the lignan fraction containing secoisolariciresinol diglycoside (SDG) and the flax
seed also reduced metastasis [70]. In another
study the flax lignan SDG was fed to mice starting 1 week after treatment with the
carcinogen dimethylbenzanthracene. The number of tumors per rat was reduced by 46%
compared to the control in this study [71]. Flax
or its lignan (SDG) were tested to see if they would prevent melanoma metastasis. The flax
or lignan fraction were fed to mice two weeks before and after injection of melanoma
cells. The flax treatment (at 2.5, 5, or 10% of diet intake) resulted in a 32, 54, and 63
percent reduction in the number of tumors, compared to the control [72]. The SDG, fed at amounts equivalent to the amount in 2.5, 5, or 10%
flax seed, also reduced the tumor number, from a median number of 62 in the control group
to 38, 36, and 29 tumors per mouse in the SDG groups, respectively [73].
More recently Thompson's research
group studied mice that were injected with human breast cancer cells. After the injection
the mice were fed a basal diet (lab mouse chow) for 8 weeks while the tumors grew. Then
one group continued the basal diet and another was fed a 10% flax seed diet. The flax seed
reduced the tumor growth rate and reduced metastasis by 45% [74].
Flax seed has been shown to
enhance mammary gland morphogenesis or differentiation in mice. Nursing dams were fed the
10% flax seed diet (or an equivalent amount of SDG). After weaning the offspring mice were
fed a regular mouse chow diet. Researchers then examined the female offspring and found an
increased number of terminal end buds and terminal ducts in their mammary glands with more
epithelial cell proliferation, all demonstrating that mammary gland differentiation was
enhanced [75]. When these female offspring were
challenged with a carcinogen to induce mammary gland tumors there were significantly lower
incidence of tumors (31% and 42% lower in the flax seed and SDG groups, respectively),
significantly lower tumor load (51% and 62% lower in the flax seed and SDG groups,
respectively), significantly lower mean tumor size (44% and 68% lower in the flax seed and
SDG groups, respectively), and significantly lower tumor number (47% and 45% lower in the
flax seed and SDG groups, respectively) [76].
So, flax seed and its lignan were able to reduce tumor growth (both in number and size of
tumors), prevent metastasis, and even cause increased differentiation of mouse mammary
tissue in suckling mice, making the offspring less susceptible to carcinogenesis even when
not consuming any flax products.
Other researchers have tested
flax seed and prostate cancer. In an animal model using mice, Lin et al [77] found that a diet supplemented with 5% flax inhibited the growth and
development of prostate cancer in their experimental mouse model. A pilot study of 25 men
who were scheduled for prostatectomy surgery were instructed to eat a low-fat diet (20% or
less of energy intake) and to supplement with 30 g of ground flaxseed per day. During the
follow-up of an average of 34 days there were significant changes in serum cholesterol,
total testosterone, and the free androgen index [78].
The mean proliferation index of the experimental group was significantly lower and
apoptotic indexes higher compared to historical matched controls. Ground flax seed may be
a very beneficial food for men battling prostate cancer. However, a meta-analysis of nine
cohort and case-control studies revealed an association between flax seed oil intake
or high blood levels of alpha-linolenic acid and prostate cancer risk [79]. It is quite likely that the lignans in flax seed are a major
component of flax's anti-cancer effects so that flax oil without the lignans is not very
beneficial. Some brands of flax seed oil retain some of the seed particulate because of
the beneficial properties of the lignans.
Fruits and
Vegetables
One of the most important
messages of modern nutrition research is that a diet rich in fruits and vegetables
protects against cancer. (The greatest message is that this same diet protects against
almost all other diseases, too, including cardiovascular disease and diabetes.) There are
many mechanisms by which fruits and vegetables are protective, and an enormous body of
research supports the recommendation for people to eat more fruits and vegetables.
Block et al [80] reviewed about 200 studies of cancer and fruit and vegetable intake. A
statistically significant protective effect of fruits and vegetables was found in 128 of
156 studies that gave relative risks. For most cancers, people in the lower quartile (1/4
of the population) who ate the least amount of fruits and vegetables had about twice the
risk of cancer compared to those who in the upper quartile who ate the most fruits and
vegetables. Even in lung cancer, after accounting for smoking, increasing fruits and
vegetables reduces lung cancer; an additional 20 to 33 percent reduction in lung cancers
is estimated [1].
Steinmetz and Potter reviewed the
relationship between fruits, vegetables, and cancer in 206 human epidemiologic studies and
22 animal studies [81]. They found "the
evidence for a protective effect of greater vegetable and fruit consumption is consistent
for cancers of the stomach, esophagus, lung, oral cavity and pharynx, endometrium,
pancreas, and colon." Vegetables, and particularly raw vegetables, were found to be
protective; 85% of the studies that queried raw vegetable consumption found a protective
effect. Allium vegetables, carrots, green vegetables, cruciferous vegetables, and tomatoes
also had a fairly consistent protective effect [81].
Allium vegetables (garlic, onion, leeks, and scallions) are particularly potent and have
separately been found to be protective for stomach and colorectal cancers [82,83]
and prostate cancer [84].
There are many substances that
are protective in fruits and vegetables, so that the entire effect is not very likely to
be due to any single nutrient or phytochemical. Steinmetz and Potter list possible
protective elements: dithiolthiones, isothiocyanates, indole-32-carbinol, allium
compounds, isoflavones, protease inhibitors, saponins, phytosterols, inositol
hexaphosphate, vitamin C, D-limonene, lutein, folic acid, beta carotene (and other
carotenoids), lycopene, selenium, vitamin E, flavonoids, and dietary fiber [81].
A joint report by the World
Cancer Research Fund and the American Institute for Cancer Research found convincing
evidence that a high fruit and vegetable diet would reduce cancers of the mouth and
pharynx, esophagus, lung, stomach, and colon and rectum; evidence of probable risk
reduction was found for cancers of the larynx, pancreas, breast, and bladder [1].
Many of the recent reports from
prospective population-based studies of diet and cancer have not found the same protective
effects of fruits and vegetables that were reported earlier in the epidemiological and
case-control studies [reviewed in [85]]. One
explanation is that people's memory of what they ate in a case-cohort study may have been
tainted by their disease state. Another problem might be that the food frequency
questionnaires (FFQ) used to measure food intake might not be accurate enough to detect
differences. Such a problem was noted in the EPIC study at the Norfolk, UK site. Using a
food diary the researchers found a significant correlation between saturated fat intake
and breast cancer, but using a FFQ there was no significant correlation [86]. So, inaccurate measurement of fruit and vegetable intake might be
part of the explanation as well.
It must be noted that upper
intakes of fruits and vegetables in these studies are usually within the range of what
people on an American omnivorous diet normally eat. In the Nurses Health Study the upper
quintiles of fruit and vegetable intake were 4.5 and 6.2 servings/day, respectively [87]. Similarly, the upper quintiles of fruit and
vegetable intake in the Health Professionals Follow-up Study were 4.3 and 5.4 serving/day
for fruits and vegetables, respectively [87].
Intakes of fruits and vegetables on the Hallelujah Diet are much higher, with median
reported intakes of six servings of fruits (646 g/day) and eleven servings of vegetables
per day (971 g/day) [88] in addition to a green
powder from the juice of barley leaves and alfalfa that is equivalent to approximately
another 100 g/day of fresh dark greens. So, it is very possible that the range of intakes
in the prospective population based studies do not have a wide enough intake on the upper
end to detect the true possible impact of a very high intake of fruits and vegetables on
cancer risk.
Cruciferous
Vegetables
Cruciferous vegetables (broccoli,
cauliflower, cabbage, Brussels sprouts) contain sulforophane, which has anti-cancer
properties. A case-control study in China found that intake of cruciferous vegetables,
measured by urinary secretion of isothiocyanates, was inversely related to the risk of
breast cancer; the quartile with the highest intake only had 50% of the risk of the lowest
intake group [89]. In the Nurses' Health Study a
high intake of cruciferous vegetables (5 or more servings/week vs less than two
servings/week) was associated with a 33% lower risk of non-Hodgkin's lymphoma [90]. In the Health Professionals Follow-up Study
bladder cancer was only weakly associated with low intake of fruits and vegetables, but
high intake (5 or more servings/week vs 1 or less servings/wk) of cruciferous vegetables
was associated with a statistically significant 51% decrease in bladder cancer [91]. Also, prostate cancer risk was found to be
reduced by cruciferous vegetable consumption in a population-based case-control study
carried out in western Washington state. Three or more servings per week, compared to less
than one serving of cruciferous vegetables per week resulted in a statistically
significant 41% decrease in prostate cancer risk [92].
Similar protective effects of cruciferous vegetables were seen in a multi-ethnic
case-control study [93]. A prospective study in
Shanghai, China found that men with detectable amounts of isothiocyanates in their urine
(metabolic products that come from cruciferous vegetables) had a 35% decreased risk of
lung cancer. Among men that had one or two genetic polymorphisms that caused them to
eliminate these isothiocyanates slower there was a 64% or 72% decreased risk of lung
cancer, respectively [94].
Broccoli sprouts have a very high
concentration of sulforophane since this compound originates in the seed and is not made
in the plant as it grows [95,96]. One sprout contains all of the sulforophane that is present in a
full-grown broccoli plant. So, if sulforophane is especially cancer-protective, it would
seem reasonable to include some broccoli sprouts in an anti-cancer diet.
Selenium
Selenium is a mineral with
anti-cancer properties. Many studies in the last several years have shown that selenium is
a potent protective nutrient for some forms of cancer. The Arizona Cancer Center posted a
selenium fact sheet listing the major functions of selenium in the body [97]. These functions are as follows:
1. Selenium is present in the
active site of many enzymes, including thioredoxin reductase, which catalyze
oxidation-reduction reactions. These reactions may encourage cancerous cells to under
apoptosis.
2. Selenium is a component of the
antioxidant enzyme glutathione peroxidase.
3. Selenium improved the immune
systems' ability to respond to infections.
4. Selenium causes the formation
of natural killer cells.
5. P450 enzymes in the liver may
be induced by selenium, leading to detoxification of some carcinogenic molecules.
6. Selenium inhibits
prostaglandins that cause inflammation.
7. Selenium enhances male
fertility by increased sperm motility.
8. Selenium can decrease the rate
of tumor growth.
A serendipitous randomized,
double-blind, controlled trial of a 200 µg/day selenium
supplement in the southeastern region of the USA (where soil selenium levels are low)
found that the primary endpoints of skin cancer were not improved by the selenium
supplement, but that other cancer incidence rates were decreased by selenium [98,99].
There was a significant reduction in total cancer incidence (105 vs 137 cases, P = 0.03),
prostate cancer (22 vs 42 cases, P = 0.005), a marginally significant reduction in
colorectal cancer incidence (9 vs 19 cases, P = 0.057), and a reduction in cancer
mortality, all cancer sites (40 vs 66 deaths, P = 0.008) (selenium versus control group
cases reported, respectively) [98]. The selenium
supplement was most effective in ex-smokers and for those who began the study with the
lowest levels of serum selenium. Several prospective studies have also examined the role
of selenium in cancer prevention, particularly for prostate cancer, summarized in Table 2.
Overall, it appears that poor
selenium levels, especially for men, are a cancer risk. If a person has low selenium
levels and other antioxidant defenses are also low the cancer risk is increased even
further. Women do not appear to be as sensitive to selenium, as breast cancer has not been
found to be influenced by selenium status in several studies [100-104], although both men and women were found to be protected by
higher levels of selenium from colon cancer [100]
and lung cancer [105,106]. Good vegetarian sources of selenium are whole grains and legumes
grown in selenium-rich soil in the western United States, brazil nuts (by far the most
dense source of selenium), nutritional yeast, brewers yeast, and sunflower seeds.
Chlorophyll
All green plants also contain
chlorophyll, the light-collecting molecule. Chlorophyll and its derivatives are very
effective at binding polycyclic aromatic hydrocarbons (carcinogens largely from incomplete
combustion of fuels), heterocyclic amines (generated when grilling foods), aflatoxin (a
toxin from molds in foods which causes liver cancer), and other hydrophobic molecules. The
chlorophyll-carcinogen complex is much harder for the body to absorb, so most of it is
swept out with the feces. The chemoprotective effect of chlorophyll and its derivatives
has been tested in laboratory cell cultures and animals [107,108]. There is so much
compelling evidence for anti-carcinogenic effects of chlorophyll that a prospective
randomized controlled trial is being conducted in Qidong, China to see if chlorophyllin
can reduce the amount of liver cancer cases, which arise from aflatoxin exposure in their
foods (corn, peanuts, soy sauce, and fermented soy beans). A 55% reduction in
aflatoxin-DNA adducts were found in the group that took 100 mg of chlorophyllin three
times a day [109]. It was supposed that the
chlorophyllin bound up aflatoxins, but there were chlorophyllin derivatives also detected
in the sera (which had a green tint to it) of the volunteers who took the supplement,
indicating a possible role in the body besides binding carcinogens in the gut [110].
Protective
Vitamins
Vitamin B-12
Vitamin B-12 has not been proven
to be an anti-cancer agent, but there is some evidence indicating that it could be
beneficial. The form of administered vitamin B-12 may be important.
Some experimental cancer studies
have been carried out with various forms of vitamin B-12. Methylcobalamin inhibited tumor
growth of SC-3 injected into mice [111], and
caused SC-3 mouse mammary tumor cells to undergo apoptosis, even when stimulated to grow
by the presence of growth-inducing androgen [112].
Methylcobalamin, but not cyanocobalamin, increased the survival time of mice bearing
implanted leukemia tumor cells [113].
5'-deoxyadenosylcobalamin and methylcobalamin, but not cyanocobalamin, were shown to be
effective cytotoxic agents [114].
Methylcobalamin also was able to increase survival time and reduce tumor growth in
laboratory mice [115].
Laboratory mechanistic evidence
for the effects of vitamin B12 were seen in a laboratory study with vitamin B-12 deficient
rats. Choi et al [116] found that the colonic
DNA of the B-12 deficient rats had a 35% decrease in genomic methylation and a 105%
increase in uracil incorporation, both changes that could increase risk of carcinogenesis.
In two prospective studies (one in Washington Country, Maryland and the Nurses' Health
Study) a relation between lower vitamin B12 status (but not deficiency) and statistically
significant higher risk of breast cancer was found [117,118]. So, there is
evidence from laboratory studies, prospective cohort studies, and mechanistic studies
showing that vitamin B-12 is an important nutrient for genetic stability, DNA repair,
carcinogenesis, and cancer therapy.
Folic Acid
Folic acid is the dark green
leafy vegetable vitamin. It has an integral role in DNA methylation and DNA synthesis.
Folic acid works in conjunction with vitamin B-6 and vitamin B-12 in the single carbon
methyl cycle. If insufficient folic acid is not available uracil is substituted for
thymidine in DNA, which leads to DNA strand breakage. About 10% of the US population (and
higher percentages among the poor) has low enough intakes of folic acid to make this a
common problem [119]. As shown in Tables 3 and 4, many studies have found a significant
reduction in colon, rectal, and breast cancer with higher intakes of folic acid and their
related nutrients (vitamin B-6 and B-12). Alcohol is an antagonist of folate, so that
drinking alcoholic beverages greatly magnifies the cancer risk of a low-folate diet.
Genetic polymorphisms (common single DNA base mutations resulting in a different amino
acid encoded into a protein) in the methylenetetrahydrofolate reductase and the methionine
synthase genes which increase the relative amount of folate available for DNA synthesis
and repair also reduces the risk of colon cancer [120-123]. Cravo et al [124] used 5 mg of folic acid a day (a
supraphysiological dose) in a prospective, controlled, cross-over study of 20 patients
with colonic adenoma polyps. They found that the folic acid could reverse DNA
hypomethylation in 7 of 12 patients who had only one polyp.
Folate may be more important for
rapidly dividing tissue, like the colonic mucosa. Therefore, the cancer risk associated
with low folate intake is probably higher for colon cancer than for breast cancer. Most of
the breast cancer studies only found a protective effect of folate among women who
consumed alcohol (see Table 4). However, among women residents of
Shanghai who consumed no alcohol, no vitamin supplements and ate unprocessed, unfortified
foods there was a 29% decreased risk of breast cancer among those with the highest intake
of folate [125]. So, there may be a true
protective effect that is masked in the western populations by so many other risk factors.
Two studies showed that the risk of cancer due to family history can be modified by high
folate intake, so a prudent anti-cancer diet would be high in dark green leafy vegetables.
The mean intake of folic acid on the Hallelujah Diet was 594 µg/day
for men and 487 µg/day for women [88].
Vitamin D
Vitamin D is produced primarily
from the exposure of the skin to sunshine. Even casual exposure of the face, hands, and
arms in the summer generates a large amount of vitamin D. In fact, simulated sunshine,
equivalent to standing on a sunny beach until a slight pinkness of the skin was detected,
was equivalent to a 20,000 IU oral dose of vitamin D2 [126]. (Note that the RDA is 400 IU for most adults.) It has been
estimated that 1,000 IU per day is the minimal amount needed to maintain adequate levels
of vitamin D in the absence of sunshine [126],
and that up to 4,000 IU per day can be safely used with additional benefit [127].
The concentration of the active
hormonal form of vitamin D is tightly regulated in the blood by the kidneys. This active
hormonal form of vitamin D has the potent anti-cancer properties. It has been discovered
that various types of normal and cancerous tissues, including prostate cells [128], colon tissue [129], breast, ovarian and cervical tissue [130], pancreatic tissue [131]
and a lung cancer cell line [132] all have the
ability to convert the major circulating form of vitamin D, 25(OH)D, into the active
hormonal form, 1,25(OH)2D. So, there is a local mechanism in many tissues of
the body for converting the form of vitamin D in the body that is elevated by sunshine
exposure into a hormone that has anticancer activity.
Indeed, 25(OH)D has been shown to
inhibit growth of colonic epithelial cells [133],
primary prostatic epithelial cells [134], and
pancreatic cells [131]. So, the laboratory work
is confirming what had been seen some time ago in ecological studies of populations and
sunshine exposure.
The mortality rates for colon,
breast, and ovary cancer in the USA show a marked north-south gradient [135]. In ecological studies of populations and sunlight exposure (no
individual data) sunlight has been found to have a protective effect for prostate cancer [136], ovarian cancer [137], and breast cancer [138].
Recently Grant found that sunlight was also protective for bladder, endometrial, renal
cancer, multiple myeloma, and Non-Hodgkins lymphoma in Europe [139] and bladder, esophageal, kidney, lung, pancreatic, rectal, stomach,
and corpus uteri cancer in the USA [140].
Several prospective studies of vitamin D and cancer have also shown a protective effect of
vitamin D (see Table 5). It could be that sunshine and vitamin D
are protective factors for cancers of many organs that can convert 25(OH)D into 1,25(OH)D2.
Antioxidants
a- and ß-Carotene and other Carotenoids
Carotenoids have been studied
vigorously to see if these colorful compounds can decrease cancer risk. In ecological
studies and early case-control studies it appeared that ß-carotene
was a cancer-protective agent. Randomized controlled trials of ß-carotene
found that the isolated nutrient was either neutral [141] or actually increased risk of lung cancer in smokers [142,143].
Beta-carotene may be a marker for intake of fruits and vegetables, but it does not have a
powerful protective effect in isolated pharmacological doses.
However, there is a large body of
literature that indicates that dietary carotenoids are cancer preventative (See Table 6). Alpha-carotene has been found to be a
stronger protective agent than its well-known isomer ß-carotene.
Studies tend to agree that overall intake of carotenoids is more protective than a high
intake of a single carotenoid. So, a variety of fruits and vegetables is still a better
anti-cancer strategy than just using a single vegetable high in a specific carotenoid.
The richest source of a-carotene is carrots and carrot juice, with pumpkins and winter
squash as a second most-dense source. There is approximately one µg
of a-carotene for every two µg of
ß-carotene in carrots. The most common sources of ß-cryptoxanthin are citrus fruits and red sweet peppers.
Lycopene
Of the various carotenoids
lycopene has been found to be very protective, particularly for prostate cancer. The major
dietary source of lycopene is tomatoes, with the lycopene in cooked tomatoes being more
bioavailable than that in raw tomatoes. Several prospective cohort studies have found
associations between high intake of lycopene and reduced incidence of prostate cancer,
though not all studies have produced consistent results [144,145]. Some studies suffer
from a lack of good correlation between lycopene intake assessed by questionnaire and
actual serum levels, and other studies measured intakes among a population that consumed
very few tomato products. The studies with positive results will be reviewed here.
In the Health Professionals
Follow-up Study there was a 21% decrease in prostate cancer risk, comparing the highest
quintile of lycopene intake with the lowest quintile. Combined intake of tomatoes, tomato
sauce, tomato juice, and pizza (which accounted for 82% of the lycopene intake) were
associated with a 35% lower risk of prostate cancer. Furthermore, lycopene was even more
protective for advanced stages of prostate cancer, with a 53% decrease in risk [146]. A more recent follow-up report on this same
cohort of men confirmed these original findings that lycopene or frequent tomato intake is
associated with about a 30–40% decrease in risk of prostate cancer, especially
advanced prostate cancer [147].
In addition to the two reports
above a nested case control study from the Health Professional Follow-up Study with 450
cases and controls found an inverse relation between plasma lycopene and prostate cancer
risk (OR 0.48) among older subjects (>65 years of age) without a family history of
prostate cancer [148]. Among younger men high
plasma ß-carotene was associated with a statistically
significant 64% decrease in prostate cancer risk. So, the results for lycopene have been
found for dietary intakes as well as plasma levels.
In a nested case-control study
from the Physicians' Health Study cohort, a placebo-controlled study of aspirin and ß-carotene, there was a 60% reduction in advanced prostate cancer
risk (P-trend = 0.006) for those subjects in the placebo group with the highest plasma
lycopene levels, compared to the lowest quintile. The ß-carotene
also had a protective effect, especially for those men with low lycopene levels [149].
In addition to these
observational studies, two clinical trials have been conducted to supplement lycopene for
a short period before radical prostatectomy. In one study 30 mg/day of lycopene were given
to 15 men in the intervention group while the 11 men were in the control group were
instructed to follow the National Cancer Institute's recommendations to consume at least 5
servings of fruits and vegetables daily. Results showed that the lycopene slowed the
growth of prostate cancer. Prostate tissue lycopene concentration was 47% higher in the
intervention group. Subjects that took the lycopene for 3 weeks had smaller tumors, less
involvement of the surgical margins, and less diffuse involvement of the prostate by
pre-cancerous high-grade prostatic intraepithelial neoplasia [150]. In another study before radical prostatectomy surgery 32 men were
given a tomato sauce-based pasta dish every day, which supplied 30 mg of lycopene per day.
After 3 weeks serum and prostate lycopene levels increaed 2-fold and 2.9-fold,
respectively. PSA levels decreased 17%, as seen also by Kucuk et al [150]. Oxidative DNA damage was 21% lower in subjects' leukocytes and 28%
lower in prostate tissue, compared to non-study controls. The apoptotic index was 3-fold
higher in the resected prostate tissue, compared to biopsy tissue [151]. These intervention studies raise the question of what could have
been done in this intervention was longer and combined synergistically with other
effective intervention methods, such as flax seed, increased selenium and possibly vitamin
E, in the context of a diet high in fruits and vegetable?
Vitamin C
Vitamin C, or ascorbic acid, has
been studied in relation to health and is the most common supplement taken in the USA. Low
blood levels of ascorbic acid are detrimental to health (for a recent article see Fletcher
et al [152]) and vitamin C is correlated with
overall good health and cancer prevention [153].
Use of vitamin C for cancer therapy was popularized by Linus Pauling. At high
concentrations ascorbate is preferentially toxic to cancer cells. There is some evidence
that large doses of vitamin C, either in multiple divided oral doses or intravenously,
have beneficial effects in cancer therapy [154-156]. Oral doses, even in multiple divided
doses, are not as effective as intravenous administration. Vitamin C at a dose of 1.25 g
administered orally produced mean peak plasma concentrations of 135 ± 21 µmol/L compared with 885 ± 201 µmol/L
for intravenous administration [154].
While vitamin C is quite possibly
an effective substance, the amounts required for these therapeutic effects are obviously
beyond dietary intakes. However, intravenous ascorbate may be a very beneficial adjuvant
therapy for cancer with no negative side effects when administered properly.
Other
Antioxidants
There are many more substances
that will have some benefit for cancer therapy. Most of these substances are found in
foods, but their effective doses for therapy are much higher than the normal concentration
in the food. For example, grape seed extract contains proanthocyanidin, which shows
anticarcinogenic properties (reviewed by Cos et al \ [157]. Also, green tea contains a flavanol, epigallocatechin-3-gallate
(EGCG), which can inhibit metalloproteinases, among several possible other mechanisms [158]. And there are claims for various other
herbal substances and extracts that might be of benefit, which are beyond the scope of
this review.
Probiotics
The bacteria that reside in the
intestinal tract generally have a symbiotic relationship with their host. Beneficial
bacteria produce natural antibiotics to keep pathogenic bugs in check (preventing diarrhea
and infections) and produce some B vitamins in the small intestine where they can be
utilized. Beneficial bacteria help with food digestion by providing extra enzymes, such as
lactase, in the small intestine. Beneficial bacteria help strengthen the immune system
right in the gut where much of the interaction between the outside world and the body goes
on. Beneficial bacteria can help prevent food allergies. They can help prevent cancer at
various stages of development. These good bacteria can improve mineral absorption,
maximizing food utilization.
However, the balance of
beneficial and potentially pathogenic bacteria in the gut is dependent on the diet.
Vegetable fiber encourages the growth of beneficial bacteria. A group of Adventist
vegetarians was found to have a higher amount of beneficial bacteria and lower amount of
potentially pathogenic bacteria compared to non-vegetarians on a conventional American
diet [159]. Differences in bacterial
populations were seen between patients who recently had a colon polyp removed,
Japanese-Hawaiians, North American Caucasians, native rural Japanese, and rural native
Africans. Lactobacillus species and Eubacterium aerofaciens, both producers
of lactic acid, were associated with the populations with the lower risk of colon cancer,
while Bacteroides and Bifidobacterium species were associated with higher
risk of colon cancer [160]
There is a solid theoretical
basis for why probiotics should help prevent cancer, especially colon cancer, and even
reverse cancer. Probiotics produce short chain fatty acids in the colon, which acidify the
environment. Lower colon pH is associated with lower incidence of colon cancer. Probiotic
bacteria reduce the level of procarcinogenic enzymes such as beta-glucuronidase,
nitroreductase, and azoreductase [161].
L. casei was used in two
trials of patients with superficial bladder cancer. In the first trial, the probiotic
group had a 50% disease free time of 350 days, compared to 195 days for the control group [162]. The second trial also showed that the
probiotics worked better than the placebo, except for multiple recurring tumors [163].
Except for the two studies noted
above, most of the research of probiotics and cancer has been done in animals. Studies
have looked at markers of tumor growth or at animals with chemically induced tumors.
Studies in rats have shown that
probiotics can inhibit the formation of aberrant crypt foci, thought to be a pre-cancerous
lesion in the colon. Some of the best results were obtained with a probiotic strain
consumed with inulin, a type of fructooligosaccharide. Total aberrant crypt foci,
chemically induced, were reduced 74% by the treatment of rats with inulin and B. longum,
but only 29 and 21% by B. longum and inulin alone, respectively [164]. There was a synergistic effect in using both products together.
Similar synergy was seen in rats with azoxymethane-induced colon cancer in another study.
Rats fed Raftilose, a mixture of inulin and oligofructose, or Raftilose with Lactobacilli
rhamnosus (LGG) and Bifidobacterium lactis (Bb12) had a significantly lower
number of tumors compared to the control group [165].
A probiotic mixture, without any prebiotic, given to rats fed azoxymethane reduced colon
tumors compared to the control (50% vs 90%), and also reduced the number of tumors per
tumor-bearing rat [166].
In lab mice bred to be
susceptible to colitis and colon cancer, a probiotic supplement, Lactobacillus
salivarium ssp. Salivarius UCC118, reduced fecal coliform levels, the number of
potentially pathogenic Clostridium perfringens, and reduced intestinal
inflammation. In this small study two mice died of fulminant colitis and 5 mice developed
adenocarcinoma in the control group of 10 mice, while there was no colitis and only 1
mouse with adenocarcinoma in the probiotic test group [167].
The research on probiotics and
disease is still an emerging field. There is a high degree of variation of health benefits
between different strains of bacteria. As new methods for selecting and screening
probiotics become available, the field will be able to advance more rapidly.
Oral Enzymes
Many people diagnosed with cancer
have digestion or intestinal tract disorders as well. Impaired digestion will greatly
hinder a nutritional approach to treating cancer. If the nutrients cannot be released from
the food and taken up by the body, then the excellent food provided by the Hallelujah Diet
will go to waste. Digestive enzyme supplements are used to ensure proper and adequate
digestion of food. Even raw foods, which contain many digestive enzymes to assist in their
digestion, will be more thoroughly digested with less of the body's own resources with the
use of digestive enzymes. So, the enzymes taken with meals do not have a direct effect
upon a tumor, but assist the body in getting all of the nutrition out of the food for
healing and restoring the body to normal function. Recently, an in vitro system was used
to test the use of supplemental digestive enzymes. The digestive enzymes improved the
digestibility and bioaccessibility of proteins and carbohydrates in the lumen of the small
intestine, not only under impaired digestive conditions, but also in healthy human
digestion [168].
There is evidence that indicates
the presence of an enteropancreatic circulation of digestive enzymes [169]. Digestive enzymes appear to be preferentially absorbed into the
bloodstream and then reaccumulated by the pancreas for use again. There appears to be a
mechanism by which digestive enzymes can reach systemic circulation.
Enzymes, especially proteases, if
they reach systemic circulation, can have direct anti-tumor activity. Wald et al [170] reported on the anti-metastatic effect of
enzyme supplements. Mice inoculated with the Lewis lung carcinoma were treated with a
proteolytic enzyme supplement, given rectally (to avoid digestion). The primary tumor was
cut out, so that the metastatic spread of the cancer could be measured. After surgical
removal of the primary tumor (day 0), 90% of the control mice died by day 18 due to
metastasized tumors. In the first group, which received the rectal enzyme supplement from
the time of the tumor-removal surgery, 30% of the mice had died from metastasized cancer
by day 25. In the second group, which received the enzymes from 6 days prior to removal of
the primary tumor, only 10% of the animals showed the metastatic process by day 15. In the
third group, which received the enzyme treatment since the initial inoculation of the
Lewis lung carcinoma, no metastatic spread of the tumor was discernible. One hundred
day-survival rates for the control, first, second, and third groups were 0, 60%, 90%, and
100%.
In a similar experiment, an
enzyme mixture of papain, trypsin, and chymotrypsin, as used in the preparation Wobe-Mugos
E, was rectally given to mice that were inoculated with melanoma cells. Survival time was
prolonged in the test group (38 days in the enzyme group compared to 24 days in the
control mice) and 3 of the 10 enzyme-supplemented mice were cured. Again, a strong
anti-metastatic effect of the proteolytic enzymes was seen [171].
Further evidence of the efficacy
of oral enzyme supplementation is available from clinical trials in Europe. Two different
studies have demonstrated that two different oral proteolytic enzyme supplements were able
to reduce high levels of transforming growth factor-ß, which
may be a factor in some cancers [172,173]. In the Slovak Republic an oral enzyme
supplement was tested in a placebo-controlled trial of multiple myeloma. For stage III
multiple myeloma, control group survival was 47 months, compared to 83 months (a 3 year
gain) for patients who took the oral enzymes for more than 6 months [174].
Enzyme supplements have also been
shown to reduce side effects of cancer therapy. Enzyme supplementation resulted in fewer
side effects for women undergoing radiation therapy for carcinomas of the uterine cervix [175], for patients undergoing radiation therapy
for head and neck cancers [176], and for
colorectal cancer patients undergoing conventional cancer treatments [177]. In a large multi-site study in Germany women undergoing
conventional cancer therapy were put into a control group or a group that received an oral
enzyme supplement. Disease and therapy related symptoms were all reduced, except tumor
pain, by the enzyme supplement. Also, survival was longer with less recurrence and less
metastases in the enzyme group [178]. In all of
these studies the oral enzyme supplements were well tolerated, with only a small amount of
mild to moderate gastrointestinal symptoms.
Even though these few studies
don't give a lot of evidence of the effectiveness of oral enzyme supplementation, it is
clear that there are some circumstances that will be helped by enzyme supplementation,
with very little danger of negative side effects. At the least, enzymes will improve
digestion and lessen the digestive burden on the body, leaving more reserves for disease
eradication. However, as the research indicates, the effect may be much greater than that,
with the potential for direct anti-tumor activity.
Whole Diet
Studies
A diet-based cancer therapy, the
Gerson Therapy, was used to treat melanoma cancer. The five-year survival rates from their
therapy compared very favorably to conventional therapy reported in the medical
literature, especially for more advanced stages of melanoma [179] (see Table 7).
An Italian cohort of 8,984 women
was followed for an average of 9.5 years, with 207 incident cases of breast cancer during
that time. Their diets were analyzed by patterns – salad vegetables (raw vegetables
and olive oil), western (potatoes, red meat, eggs and butter), canteen (pasta and tomato
sauce), and prudent (cooked vegetables, pulses, and fish). Only the salad vegetable diet
pattern was associated with a significantly lower risk of breast cancer, about 35% lower.
For women of normal weight (BMI <25) the salad vegetable pattern was even more
protective, about a 61% decreased risk of breast cancer [180]. The overall dietary pattern does make a very significant
difference.
In US-based studies the
"prudent" diet has been shown to be protective for colon cancer, while the
"western" diet has been shown to be detrimental. The "western" dietary
pattern, with its higher intakes of red meat and processed meats, sweets and desserts,
French fries, and refined grains, was associated with a 46% increase relative risk of
colon cancer in the Nurses' Health Study [45].
Slattery et al [17] found a two-fold increase in
relative risk of colon cancer associated with a "western" dietary pattern, and a
35–40% decrease in relative risk associated with the "prudent" pattern,
especially among those diagnosed at an earlier age (<67 years old). The "salad
vegetable" pattern is still more likely to be protective compared to the prudent
dietary pattern, but this pattern did not exist in this study population.
In an analysis of the colon
cancer data from the Health Professionals Follow-up Study, Platz et al [56] found that there was a 71% decrease in colon cancer risk when men with
none of six established risk factors were compared to men with at least one of these risk
factors (obesity, physical inactivity, alcohol consumption, early adulthood cigarette
smoking, red meat consumption, and low intake of folic acid from supplements). So, if all
men had the same health profile as these healthier 3% of the study population, colon
cancer rates would have been only 29% of what they measured.
A plant-based dietary pattern in
being currently tested in the Women's healthy Eating and Living (WHEL) Study. About 3,000
women who were treated for an early stage of breast cancer have been randomized into two
groups. The dietary goals for the test group of the study are 5 servings of vegetables, 16
oz of vegetable juice, 3 servings of fruit, 30 g of fiber, and <20% of energy from fat.
No guidelines were given for animal product intake, and initial results seem to confirm,
since there were no changes in body weight, total cholesterol, or LDL cholesterol [181], which would be affected by animal protein
intake. However, over the first year of follow-up vegetable intake did increase to seven
servings/day, fruit intake increased to 3.9 servings/day, energy from fat decreased from
28% to 23%. Also, plasma carotenoid concentrations increased significantly in the
intervention group, but not in the control group. a-Carotene
increased 223%, ß-carotene increased 87%, lutein increase
29%, and lycopene increased 17% [182],
indicating that a substantial dietary change had been made by these women. It will be very
interesting to follow the results of this study.
Conclusions
What is the result when all of
these things are put together? What if all of these factors reviewed here were taken into
account and put into practice? This anticancer diet would have:
• adequate, but not excessive calories,
• 10 or more servings of vegetables a day,
including cruciferous and allium vegetables; vegetable juice could meet part of this goal,
• 4 or more servings of fruits a day,
• high in fiber,
• no refined sugar,
• no refined flour,
• low in total fat, but containing
necessary essential fatty acids,
• no red meat,
• a balanced ratio of omega 3 and omega 6
fats and would include DHA,
• flax seed as a source of phytoestrogens,
• supplemented with ~200 µg/day selenium,
• supplemented with 1,000 µg/day methylcobalamin (B-12),
• very rich in folic acid (from dark green
vegetables),
• adequate sunshine to get vitamin D, or
use 1,000 IU/day supplement,
• very rich in antioxidants and
phytochemicals from fruits and vegetables, including a-carotene,
ß-carotene, ß-cryptoxanthin,
vitamin C (from foods), vitamin E (from foods),
• very rich in chlorophyll,
• supplemented with beneficial probiotics,
• supplemented with oral enzymes
As reviewed above, reductions of 60 percent in
breast cancer rates have already been seen in human diet studies, and a 71 percent
reduction in colon cancer for men without the known modifiable risk factors. These
reductions are without taking into account many of the other factors considered in this
review, such as markedly increased fruit and vegetable intake, balanced omega 3 and 6
fats, vitamin D, reduced sugar intake, probiotics, and enzymes – factors which all
are likely to have an impact on cancer. Certainly cancer prevention would be possible, and
cancer reversal in some cases is quite likely.
Competing
Interests
Michael Donaldson is a research
scientist at the Hallelujah Acres Foundation, a foundation for investigations pertaining
to the Hallelujah Diet. Funding for this review was provided by the Hallelujah Acres
Foundation.
Author
Michael S Donaldson - Director of Research, Hallelujah Acres Foundation, 13553
Vantage Hwy, Ellensburg, WA 98926, USA
Nutrition Journal 2004, 3:19 doi:10.1186/1475-2891-3-19
© 2004 Donaldson; licensee BioMed Central Ltd.
This is an open-access
article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited.
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