Dr. Johanna Budwig’s Healing Diet & Protocol (4)

Effects of Flaxseed and Flaxseed Components (Lignan, Lignan Precursors & Oil) on Cancer and Tumor Growth

Research Studies on Animals AND Humans

Continuing from the first page devoted to studies into flaxseed and its components and cancer, this page lists further research possibly validating an anticancer effect of these compounds. Please also note the important addendum at the bottom of the page.

3 A 1996 animal experiment aiming "to determine whether supplementation with flaxseed, its lignan or oil fractions, beginning 13 weeks after carcinogen administration, would reduce the size of established mammary tumors (present at the start of treatment) and appearance of new tumors in rats" concluded that "the S.D. in flaxseed appears to be beneficial throughout the promotional phase of carcinogenesis whereas the oil component is more effective at the stage when tumors have already been established."

Flaxseed and its lignan and oil components reduce mammary tumor growth at a late stage of carcinogenesis.
Thompson LU, Rickard SE, Orcheson LJ, Seidl MM. Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Ontario, Canada.
Flaxseed, a rich source of mammalian lignan precursor secoisolariciresinol- diglycoside (S.D.) and alpha-linolenic acid (ALA), has been shown to be protective at the early promotion stage of carcinogenesis. The objective of this study was to determine whether supplementation with flaxseed, its lignan or oil fractions, beginning 13 weeks after carcinogen administration, would reduce the size of established mammary tumors (present at the start of treatment) and appearance of new tumors in rats. Dietary groups consisted of the basal diet (BD, 20% corn oil) alone or supplemented with a gavage of 2200 nmol/day S.D. [S.D., equal to level in 5% flaxseed (F)], 1.82% flaxseed oil (OIL, equal to level in 5% F) or 2.5% or 5% flaxseed (2.5% F and 5% F, respectively). After 7 weeks of treatment, established tumor volume was over 50% smaller in all treatment groups (OIL, 2.5% F, 5% F, P < 0.04; S.D., P < 0.08) while there was no change in the BD group. New tumor number and volume were lowest in the S.D. (P < 0.02) and 2.5% F (P < 0.07) groups. The combined established and new tumor volumes were smaller for the S.D., 2.5% F and 5% F groups (P < 0.02) compared to the OIL and BD groups. The high negative correlation (r = -0.997, P < 0.001) between established tumor volume and urinary mammalian lignan excretion in the BD, S.D., 2.5% F and 5% F groups indicates that the reduction in tumor size is due in part to the lignans derived from the S.D. in flaxseed. However, there was no relationship between new or total tumor development and urinary lignan levels. The effect of flaxseed oil may be related to its high ALA content. In conclusion, the S.D. in flaxseed appears to be beneficial throughout the promotional phase of carcinogenesis whereas the oil component is more effective at the stage when tumors have already been established.
The original NCBI report with references

4 A 1992 animal experiment aiming to determine "whether flaxseed decreases the risk for colon carcinogenesis" concluded that while the observed effects were "not linearly related to the level of flaxseed fed, it suggests that flaxseed feeding may reduce the risk for colon carcinogenesis".

Flaxseed supplementation and early markers of colon carcinogenesis. Serraino M, Thompson LU. Department of Nutritional Sciences, University of Toronto, Ontario, Canada.
Since flaxseed ingestion produces potentially anticarcinogenic lignans in the colon, this study determined whether flaxseed decreases the risk for colon carcinogenesis. Following a single injection of azoxymethane (15 mg/kg body wt.), five groups of male Sprague-Dawley rats were fed a high-fat (20% corn oil) basal diet with or without supplementation with 5% or 10% flaxseed meal (FM) or flaxseed flour (FF) for four weeks. Upon sacrifice, colons were examined for aberrant morphology and cell proliferation. In the descending colon of supplemented groups, the total number of aberrant crypts and foci were significantly reduced by 41-53% and 48-57%, respectively. The labeling index (LI) was also 10-22% lower in these groups, except for the 5% FM group. While these effects are not linearly related to the level of flaxseed fed, it suggests that flaxseed feeding may reduce the risk for colon carcinogenesis.
The original NCBI report with references

5 A 1991 animal experiment tested flaxseed for its effect on early markers of risk for mammary carcinogenesis:

The effect of flaxseed supplementation on early risk markers for mammary carcinogenesis.
Serraino M, Thompson LU. Department of Nutritional Sciences, University of Toronto, Ontario, Canada.
Since lignans have been suggested to have some cancer-protective effects, flaxseed, the most abundant source of lignan precursors, was tested for its effect on early markers of risk for mammary carcinogenesis. Supplementation of a high-fat diet with flaxseed flour (FF) or defatted flaxseed meal (FM) (5% or 10%) reduced the epithelial cell proliferation by 38.8-55.4% and nuclear aberrations by 58.8-65.9% in female rat mammary gland, with optimum effects seen with the 5% FF.
These protective effects were accompanied by increases in urinary lignan excretion indicating that they may be related to the ability of flaxseed to provide lignan precursors.
The original NCBI report with references

6 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

7 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

8 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

9 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

10 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

11 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

12 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)

Healing Cancer Naturally's stance on animal experimentation

Personally, I don’t advocate animal experiments for the reasons sketched below. I will occasionally include pertinent research however (since it has been and unfortunately still will be done in any case), as I have done above for instance 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 here about the detailed scientific arguments and the serious fundamental implications that the issue of animal experimentation & product safety testing based on animal models has for everyone’s health, recovery and safety, making it a possible matter of life or death for many. I personally know someone who has been seriously ill, incapacitated and partially wheelchair-bound for over a decade after using a household cleaner containing a compound which had been tested “safe” for humans on animals.

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