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Dr. Budwig • Dr. Budwig‘s Major Discovery • Books • Cancer Cure Testimonials
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For the most part one cannot expect the doctors to place any real
credibility to the use of FO/CC [flax oil and cottage cheese]. It seems incredible that anything could be successful other than what they are taught in Med school. Imagine the blow to one's ego if it became official
that something with which he or she is not familiar would be found to be much better than the things that were studied 10 years to learn.
Cliff Beckwith
More on Dr. Budwig’s Healing Diet & Protocol
Welcome to this fourth page devoted to the discoveries of Dr. Johanna Budwig on the subject of healing cancer naturally! This
page lists further research studies into the effects of flaxseed and flaxseed components on cancer and tumor growth.
For a thorough introduction to the subject, see Dr. Budwig’s Healing Protocol page 1, including the complete list of Healing Cancer Naturally articles on Dr. Budwig’s protocol.
Research S
tudies on Animals & Humans into the Effects of Flaxseed and Flaxseed Components (Lignan, Lignan Precursors & Oil) on Cancer and Tumor Growth*
ctd. from previous page
An animal experiment testing a lignan precursor isolated from flaxseed ”for effects on mammary tumorigenesis in rats fed a high-fat (20%) diet...
showed, for the first time, that [the lignan precursor] has an antitumor effect when provided at the early promotion stage of tumorigenesis”.
Antitumorigenic effect of a mammalian lignan precursor from flaxseed.
Thompson LU, Seidl MM, Rickard SE, Orcheson LJ, Fong HH. Department of Nutritional Science, Faculty of Medicine, University of Toronto, Ont, Canada.
Secoisolariciresinol diglycoside (SD), a mammalian lignan precursor found in high-fiber foods, was isolated from flaxseed and tested for effects on mammary
tumorigenesis in rats fed a high-fat (20%) diet. Ingestion of purified SD at 1.5 mg/day for 20 weeks starting 1 week after treatment with the carcinogen
dimethylbenzanthracene resulted in a 37% reduction (p < 0.05) in the number of tumors per tumor-bearing rat and a 46% reduction (p < 0.05) in the number of
tumors per tumor-bearing rat and a 46% reduction (p < 0.05) in the number of tumors per number of rats in each group. Urinary mammalian lignan excretion
significantly increased (p < 0.0001) with SD treatment, indicating the conversion of SD to mammalian lignans. No enlargement or gross abnormalities of the major
organs were observed in the SD-treated rats. This study showed, for the first time, that SD has an antitumor effect when provided at the early promotion stage of
tumorigenesis and may contribute to the health benefits of high-fiber foods.
The original NCBI report with references
An animal experiment testing “[s]uppression of tumor growth and metastasis by dietary fish oil combined with vitamins E and C and
cisplatin” concluded that “[d]iets enriched with omega-3 PUFA [polyunsaturated fatty acids] may have beneficial anticancer effects in particular when containing only basal amounts of antioxidants such as vitamin E or C”. [D
ietary fish oil is the richest non-vegetarian source of omega-3 polyunsaturated fatty acids, as is flaxoil as a vegetarian source.]
Suppression of tumor growth and metastasis by dietary fish oil combined with
vitamins E and C and cisplatin.
Yam D, Peled A, Shinitzky M. Department of Biological Chemistry, The Weizmann Institute of Science, Rehovot, Israel.
PURPOSE:
The anticancer activity of omega-3 polyunsaturated fatty acids (omega-3 PUFA) has been shown in a large number of studies. This study was undertaken to analyze the
combined effect of omega-3 PUFA and antioxidative vitamins on the level of spontaneous metastatic dissemination. The supportive effect of this dietary combination on chemotherapy with cisplatin (CP) was determined in parallel.
METHODS:
C57BL/6J mice bearing the Lewis lung carcinoma 3LL were fed ad libitum one of three isocaloric diets containing 5% soybean oil supplemented with 40 mg/kg
alpha-tocopherol acetate (SO diet), or 4% fish oil plus 1% corn oil, and basal amounts of vitamin E (FO diet) or FO diet supplemented with vitamins E and C
(FO+E+C diet). These diets were tested in combination with the conventional cytotoxic agent CP in a series of regimens. Tumor growth, feed consumption, body weight, lung metastasis and lung histology were followed.
RESULTS:
Both the FO dietary groups showed significantly lower tumor development than the SO group in all examined parameters, indicating that omega-3 PUFA have anticancer activity.
However, the FO diet, in comparison with the FO+E+C diet induced a significantly slower rate of tumor growth, and lower metastatic load, as reflected in lung weight.
The decrease in the anticancer activity of FO by the addition of vitamins E and C suggests that in situ oxidation of omega-3 PUFA underlies their anticancer action.
It is thus proposed that oxidized omega-3 PUFA accumulates in the membranes and the cytosol of tumor cells, reducing their vitality and eventually leading to their death.
No signs of anorexia or cachexia were observed in either FO group, in contrast to the SO group. CP treatment with the SO diet had no apparent therapeutic effect, while with the FO diets it reduced the metastatic load.
The best regimen of this combined treatment was FO diet followed by CP treatment with FO diet supplemented with vitamins E and C after resection of the primary growth.
This regimen could be translated to a combined therapy for human cancer.
CONCLUSIONS:
Diets enriched with omega-3 PUFA may have beneficial anticancer effects in
particular when containing only basal amounts of antioxidants such as vitamin E or C. Furthermore, the addition of drugs which promote oxidation of omega-3 PUFA, such
as ferrous salts (e.g. as prescribed for the treatment of anemia), may further increase these effects. However, the supportive effect of omega-3 PUFA in
chemotherapy (e.g. with CP) increases when vitamins E and C are also included.
The original NCBI report with references
An animal experiment testing “the influence of dietary flaxseed and other grains, fruits and vegetables on the frequency of spontaneous
chromosomal damage in mice” concluded that “at least one class of spontaneous genetic damage can be modified by diet and suggests that short-term experiments with small numbers of animals can be
used to identify dietary anticarcinogens that may influence human cancer rates.”
The influence of dietary flaxseed and other grains, fruits and vegetables on the
frequency of spontaneous chromosomal damage in mice.
Trentin GA, Moody J, Torous DK, Thompson LU, Heddle JA., Department of Biology, York University, 4700 Keele Street, Toronto, Ont., Canada M3J 1P3.
Spontaneous genetic damage, whether mutations or chromosomal aberrations, undoubtedly arise from a variety of sources including replication errors, oxidative
damage, background radiation, and chemical exposure. Given the numerous correlations between diet and cancer, it seemed possible that diet could influence the
spontaneous rate of DNA damage and its genetic consequences. Since diets high in vegetables, fruits, and grains are associated with lower rates of cancer, we
supplemented the diets of mice and measured the frequency of micronuclei in the peripheral blood. Micronuclei arise from broken chromosomes or chromosome loss in
the erythroblast. They are first seen in the short reticulocyte stage of the red blood cell but persist for the entire 30-day lifespan of the cell in mice. C57Bl mice were
placed on a defined diet (AIN-93G) supplemented to 20% final dry weight with grains or freeze-dried fruits or vegetables. The micronucleus frequency was measured in a
pre-exposure blood sample and every 2 weeks thereafter for 6 weeks. This was possible in spite of the low spontaneous frequency of 1/1000-2/1000 cells by the use
of a novel flow cytometric method, which permitted the analysis of both the mature red blood cells and reticulocytes. Of the foods tested, flaxseed proved to be the most
protective by reducing the incidence of micronuclei in both the reticulocyte and normochromatic erythrocyte cell populations by 30 and 11%, respectively. The results
show that at least one class of spontaneous genetic damage can be modified by diet and suggests that short-term experiments with small numbers of animals can be
used to identify dietary anticarcinogens that may influence human cancer rates.
The original NCBI report with references
Lignans and tamoxifen, alone or in combination, reduce human breast cancer cell adhesion, invasion and migration in vitro.
Chen J, Thompson LU., Department of Nutritional Sciences, Faculty of Medicine,
University of Toronto, Toronto, Ont., Canada.
Flaxseed has been shown to reduce the metastasis of estrogen receptor negative (ER-) human breast cancer in nude mice. This study determined whether enterodiol
(ED) and enterolactone (EL), metabolites of plant lignans exceptionally rich in flaxseed, and tamoxifen (TAM), alone or in combination, can influence the various
steps of metastasis, that is, breast cancer cell adhesion, invasion and migration, of two ER- human breast cancer cell lines, MDA-MB-435 and MDA-MB-231. The
inhibition by ED, EL or TAM (1-5 microM) of cell adhesion to Matrigel or extracellular matrices, fibronectin, laminin, and type IV collagen, as well as cell invasion was dose
dependent in both cell lines. When ED, EL and TAM were combined at 1 microM, a greater inhibitory effect on cell adhesion and invasion was observed than with either
compound alone. ED and EL at doses of 0.1-10 microM reduced cell migration, but TAM had no effect at 0.1 and 1 microM, and exhibited a stimulatory effect at 10
microM. It is concluded that lignans and TAM, alone or in combination, can inhibit the steps involved in the metastasis cascade. Although more investigations are required,
the study also suggests that the intake of the lignan-rich flaxseed may not antagonize the effect of TAM in ER- breast cancer cells.
The original NCBI report with references
Pilot study to explore effects of low-fat, flaxseed-supplemented diet on proliferation of benign prostatic epithelium and prostate-specific antigen
Demark-Wahnefried W, Robertson CN, Walther PJ, Polascik TJ, Paulson DF, Vollmer
RT., Division of Urologic Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA.
OBJECTIVES: Dietary factors may influence the prostate and have an impact on
prostatic growth and disease. A small number of studies have suggested that flaxseed-supplemented, fat-restricted diets may thwart prostate cancer growth in
both animals and humans. Unknown, however, is the potential effect of such a diet on benign prostatic epithelium. METHODS: We undertook a pilot study to explore
whether a flaxseed-supplemented, fat-restricted diet affects the proliferation rates in benign epithelium. We also explored the effects on circulating levels of
prostate-specific antigen (PSA), total testosterone, and cholesterol. Fifteen men who were scheduled to undergo repeat prostate biopsy were instructed to follow a low-fat
(less than 20% kcal), flaxseed-supplemented (30 g/day) diet and were provided with a supply of flaxseed to last throughout the 6-month intervention period. The PSA,
total testosterone, and cholesterol levels were determined at baseline and at 6 months of follow-up.
Reports from the original and repeat biopsies were compared, and proliferation
(MIB-1) rates were quantified in the benign prostatic epithelium. RESULTS: Statistically significant decreases in PSA (8.47 +/- 3.82 to 5.72 +/- 3.16 ng/mL; P =
0.0002) and cholesterol (241.1 +/- 30.8 to 213.3 +/- 51.2 mg/dL; P = 0.012) were observed. No statistically significant change was seen in total testosterone (434.5 +/-
143.6 to 428.3 +/- 92.5 ng/dL). Although 6-month repeat biopsies were not performed in 2 cases because of PSA normalization, of the 13 men who underwent
repeat biopsy, the proliferation rates in the benign epithelium decreased significantly from 0.022 +/- 0.027 at baseline to 0.007 +/- 0.014 at 6 months of follow-up (P = 0.0168).
CONCLUSIONS: These pilot data suggest that a flaxseed-supplemented, fat-restricted diet may affect the biology of the prostate and associated biomarkers. A randomized
controlled trial is needed to determine whether flaxseed supplementation, a low-fat diet, or a combination of the two regimens may be of use in controlling overall prostatic growth.
The original NCBI report with references
An animal experiment testing “the effect of flaxseed (FS), the richest source of lignans and alpha-linolenic acid, on growth and metastasis
of established human breast cancer in a nude mice model” concluded that “flaxseed inhibited the established human breast cancer growth and metastasis in a nude mice model, and this effect is partly due to
its downregulation of insulin-like growth factor I and epidermal growth factor receptor expression”.
Dietary flaxseed inhibits human breast cancer growth and metastasis and
downregulates expression of insulin-like growth factor and epidermal growth factor receptor.
Chen J, Stavro PM, Thompson LU., Department of Nutritional Sciences, Faculty of
Medicine, University of Toronto, Toronto, ON, Canada M5S 3E2.
Recent studies indicate that diets rich in phytoestrogens and n-3 fatty acid have
anticancer potential. This study determined the effect of flaxseed (FS), the richest source of lignans and alpha-linolenic acid, on growth and metastasis of established
human breast cancer in a nude mice model. Estrogen receptor-negative human breast cancer cells, MDA-MB-435, were injected into the mammary fat pad of mice
(Ncr nu/nu) fed a basal diet (BD). At Week 8, mice were randomized into two diet groups, such that the groups had similar tumor size and body weight. One continued
on the BD, while the other was changed to BD supplemented with 10% FS, until sacrifice at Week 15. A significant reduction (P < 0.05) in tumor growth rate and a
45% reduction (P = 0.08) in total incidence of metastasis were observed in the FS group. Lung metastasis incidence was 55.6% in the BD group and 22.2% in the FS
group, while the lymph node metastasis incidence was 88.9% in the BD group and 33.3% in the FS group (P < 0.05). Mean tumor number (tumor load) of total and
lymph node metastasis was significantly lower in the FS than in the BD group (P < 0.05).
Metastatic lung tumor number was reduced by 82%, and a significantly lower tumor
trend (P < 0.01) was observed in the FS group. Lung weight, which also reflects metastatic tumor load, in the FS group was reduced by 20% (P < 0.05) compared with the BD group.
Immunohistochemical study showed that Ki-67 labeling index and expression of insulin-like growth factor I and epithelial growth factor receptor in the primary tumor
were lower in the FS (P < 0.05) than in the BD group. In conclusion, flaxseed inhibited the established human breast cancer growth and metastasis in a nude mice
model, and this effect is partly due to its downregulation of insulin-like growth factor I and epidermal growth factor receptor expression.
The original NCBI report with references
An animal experiment showed that “supplementation of 10% flaxseed, the richest source of mammalian lignans, to nude mice with
established human breast tumors reduced tumor growth and metastasis”.
Flaxseed inhibits metastasis and decreases extracellular vascular endothelial growth
factor in human breast cancer xenografts.
Dabrosin C, Chen J, Wang L, Thompson LU., Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, 150 College Street, ON, M5S 3E2, Toronto, Canada.
Angiogenesis is important in tumor growth, progression and metastatic dissemination. Vascular endothelial growth factor (VEGF) is one key factor in
promotion of breast cancer angiogenesis. VEGFs are bioactive in the extracellular space where they become available to the endothelial cells. Phytoestrogens such as
lignans have been shown to alter breast cancer incidence and be cancer-protective in rats. We show that supplementation of 10% flaxseed, the richest source of
mammalian lignans, to nude mice with established human breast tumors reduced tumor growth and metastasis. Moreover, flaxseed decreased extracellular levels of
VEGF, which may be one mechanistic explanation to the decreased tumor growth and metastasis.
The original NCBI report with references
If you key in "flaxseed cancer" at PubMed, you'll find dozens of studies validating Dr. Budwig’s conclusions. These studies, however, appear to go nowhere past nude mice studies because--duh!--no one
wants to fund further studies on humans. Not profitable. (C.C., Long Beach, CA)
*Note by Healing Cancer Naturally:
Personally, I don’t advocate animal experiments for reasons outlined below. I am including the above pertinent research however (since it has been done in any case)
in support of the efficacy of the “Budwig diet” for those who believe that test results are transferrable to human beings (and to my knowledge they occasionally are).
More generally speaking, animal experiments could justifiably be called “as useless and dangerous for humans as cruel to animals” (e.g. thalidomide was tested safe on
rats while penicillin would have never been allowed for human consumption had it initially been tested on guinea pigs or hamsters, since it kills those species!). For a good summary re ”Does animal testing help human medicine
?” see for instance www.saav.org.za, and for thalidomide & an entire online book on the subject of 'ANIMAL RESEARCH TAKES LIVES - Humans and Animals BOTH Suffer' see www.health.org.nz.
Dr Irwin D Bross PhD writes, “There is no good factual evidence to show that the use of animals in cancer research has led to the prevention or cure of a single human cancer.” Full quote of Dr Bross and others under On Cancer Research.
There are better alternatives that do not involve cruelty to animals and give much more reliable results for humans (such as tests performed on human cell cultures).
These humane and solely reliable test methods just need to be implemented, and if a sufficiently large part of the public calls for them, they will be applied - to everyone’s benefit! Please consider joining this call!
The subject of cancer research based upon animal models of human
disease is in fact of such major importance that Healing Cancer Naturally now devotes many pages to it. Learn about the detailed scientific arguments and the fundamental implications of the issue of animal
experimentation for everyone’s health, recovery and safety, making it a possible matter of life or death for many,
here.
Success Story: Cancer and Ferrets - Adrenal Cancer GONE!
by Robb T.
Anyone that owns ferrets knows that ferrets get do really bad when fed milk products. Although they 'love' milk products, many ferret
owners have found out that they usually end up with a bad case of diarrhea. So in general we do not feed milk products to ferrets.
Ferrets are able to eat some veggies, but are mainly protein eaters. Anyone that owns ferrets also knows that they are very susceptible
to adrenal cancer. When they start going downhill from adrenal cancer, their hair starts to fall out, and you end up with essentially a bald looking ferret.
This is quite common and accounts for in my own guestimate about 80% of the deaths out there with ferrets. So when a ferret is old,
and its hair starts to fall out, you know that the animal is a write-off.
Our ferret was totally BALD from its neck down to its two front paws. It was bald on the top of its neck back to its shoulders. The
patches were growing in size, and I could see that the hair on its tail was starting to fall off. Every ferret owner told us that our family pet has adrenal cancer.
Ferrets are in general fed a high protrein diet and if you are a knowledgable owner you usually give the ferret an Omega 3 fatty
acid supplement (usually ferretone is one such brand).
But for some reason, ferrets still keep coming down with adrenal cancer.
After studying the Budwig protocol we see:
Cottage Cheese - Sulphurated Amino Acids = Sulphonyl and Protein.
Flaxseed Oil - The Omega 3 fatty acid source.
Fruits - The Vitamin C source.
The 'standard' ferret diet consists of:
High Protein Kibble - The protein source.
Ferretone - The omega 3 fatty acid source and vitamin C source.
We can see from the above menu that the only thing missing is the sulphonyl.
So with NO OTHER CHANGES IN DIET OR ENVIRONMENT, all we did was add sulphonyl in the form of MSM to the ferret’s water supply.
This did the trick and in 4 weeks the changes in our ferret’s condition were massive and obvious. There is no denying the changes, and it
got even my wife to start taking MSM (hates the taste) on a regular basis.
It's been about 7-8 weeks now, and the ferret has grown all its hair back, and has NO VISIBLE SIGNS OF ADRENAL CANCER. Side
effects include softer hair, and lots of it. It also appears to be more gentle at play with the other ferrets.
We will be adding sulphonyl to the ferret’s water supply for ever so we won't have to go through this again. We will also continue to take
sulphonyl in our daily diets.
At our household we humans generally take about 1 to 4 tablespoons (1 tablespoon = 10 1000 mg MSM tablets if my conversion is correct) each day.
I've been on it for about 6 months to a year now, and feel great. We buy MSM in bulk. If you are really sick, you may want to ramp your
dose up so as to minimize the resulting healing crisis. It is my most humble opinion that 3 tablets a day is not enough!
More information on MSM
Most of my information about MSM comes from an audio called "The MSM Miracle". I found the details on the net about MSM to be fairly
sketchy, or hard to locate on the net.
What is it that MSM does. Sulphonyl in MSM is quite simply another protein bonder just like Vitamin C. If you don't get enough Vitamin
C, your proteins all fall apart and you bleed to death internally. Doctors call that scurvy.
Sulphonyl is the other half of vitamin C. While vitamin C is responsible for bonding protein in a non-flexible way. MSM in the
'flexible' bond between protein. Some older bottles of MSM that I picked up at health food story simply said 'healthy tissue'. People normally would never connect the dots. Let me explain it in a
manner that would 'turn the lights on'.
Let’s explain it this way. It’s like when you’re building a cement wall. If you don't use any rebar or chicken wire, it might need to be 10
feet thick in order to stand up. But if you so much as look at funny it will fall apart because it doesn't have any strength.
If you have some rebar in the wall, then the wall can be thinned out to 5 feet wide. But if you flex the wall at all it will be brittle and
crack. But it will hold together reasonably well.
If you add lots and lots of chicken wire to the wall, then you can make the same wall say only 1 foot thick. You can bend it and it will
stay together much better than both previous walls. So this wall that is only 1 foot thick is 'stronger' than the previous two walls.
Now say that some guy is using a pick to take the wall apart. Quite obviously the wall with all the chicken wire and rebar is going to be a
lot harder to take apart.
Now let’s say that wall is a lung membrane. Which version of the wall is going to pass out carbon dioxide the best. Which is going to
allow the most oxygen back in? Mirror this thought to the membranes in your intestines.
Mirror this thought to a gland that produces enzymes. Everything works on membranes. All the cells pass out toxins, pull in nutrients
through membranes. So increased MSM intake over time, results in thinning, more permeable membranes, as the lecture asserts.
Now picture a white blood cell or T cell. If it's made out of rebar and chicken wire it will be able to kill off 10 times the bacteria and
viruses of a standard person that is not on regular doses of sulphonyl. These studies were done with Garlic as the sulphonyl source {DMSO}.
Now picture the guy with the pick as being a liver fluke living in the pancreas or some other tissue. Which tissue is going to be 'easier' for
the parasite to live in? Now factor in living with the above noted super stong which blood cell nipping at the liver fluke’s heels.
The body is made up of 1/3 of sulphonyl compounds.
"The MSM Miracle" asserts that cancer is nothing more than another form of a sulphonyl deficiency. Meanwhile, we hang out in this area
talking about taking our suphurated amino acids, and the dots start to correlate and connect.
So the cottage cheese also contains amino acids. These amino acids are the protein source. So we have the cement entering the body.
When you study what Omega 3 fatty acid actually does, we see even more about what Budwig was up to. Omega 3 fatty acid is the final
part of the humanization of proteins. Unheated omega 3 makes the protein that you eat available to your body so it actually gets to use it. Heated Omega 3 fatty acid takes protein AWAY from your body
(by releasing free radicals ). Hence no omega 3 fatty acid, no available cement! Flaxseed oil provides the critical omega 3 fatty acids, and poof, the cement becomes available.
Even more about what Budwig was up to starts to surface.
We also need a Vitamin C. The fruits and veggies of the diet provided the Vitamin C source. The rebar!
So all that Budwig was doing is making a HIGH QUALITY protein available that is easy to digest, and fix the sulphonyl deficiency in the diet.
It all works the same way from ferrets, to cats, to dogs, to rats, to humans. In the case of my ferret, I didn't use flaxseed oil. I didn't
use fresh fruits. I didn't even use cottage cheese! But as far as I am concerned I did a form of Budwig on him! Some may object, or disagree with me on this statement, others may not. It's up to one's own opinion.
Buying MSM in bulk
I just pick it up from a local health food store. Currently prices for MSM where I am is $40.00 CDN per kg in bulk. In non-bulk, I can
get it locally from the health food store for about $28.00 per 0.3 kgs. So as you can well imagine the cost drops drastically when you can get it in bulk. But even at non-bulk prices, it is fairly cheap. But
of course at the levels that my houshold and ferrets go through the stuff, it could get kinda expensive.
Vegan Alternatives • Why Organic Dairy
Quotes • Research • Cancer Cure Testimonials • Tips
Comments • Budwig Diet Details • FAQ • Lignan or Plain Flaxseed Oil
Dr. Johanna Budwig • Dr. Budwig‘s Major Discovery • Books in English & German
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