Breast Cancer Choices  
Scrutinizing the evidence for breast
cancer procedures and treatments

    Editor's Note: Using the screening iodine-loading test, a small preliminary breast cancer-
    iodine study found that there is a significant decrease in excretion of urinary iodine in
    role in breast cell differentiation.

    Identification of Breast Cancer by Differences in Urinary Iodine
    (Abstract Number: 2150)96th Annual Meeting AACR, April 16-20, 2005, Anaheim/Orange
    County, CA By Bernard A. Eskin, Waqas Anjum, Guy E. Abraham, Frederick Stoddard,
    Ann Prestrud, Ari D. Brooks, Drexel University College of Medicine, Philadelphia, PA,
    Optimox Corporation, Torrance, CA.

    Introduction: Iodine is involved metabolically in normal, nursing, and neoplastic breast
    tissues.  Our objective was to evaluate differences in urinary iodine levels in women with
    benign and malignant breast changes.  Methods:  Ninety-eight women with a median
    age of 47 years (range 15-87) presenting with benign or malignant breast diagnoses to
    the university breast center participated in this study.  Women with a history of
    hyper/hypothyroidism were excluded.  Urine specimens were collected following
    informed consent.  Urine was quantified by chromatography/anion exchange resin.  
    Values are reported as micrograms (mcg) iodine or milligrams (mg) bromide per liter by
    ion selective electrode assay.  A t-test was used to compare means.  Results:  Our final
    cohort included 20 women with cancer (DCIS=6, invasive cancer=14), 20 women who
    were smokers and 42 who were post menopausal.
    A significant difference in iodine excretion between women with cancer (105 mcg/l)
    versus non-cancer (141 mcg/l, p<0.05) was demonstrated.
    Trends seen were: 1) Higher excretion (26%) in postmenopausal versus
    premonopausal women (152 mcg/l vs. 121 mcg, p=NS). 2) Smokers had lower (23%)
    iodine excretion (109 mcg/l vs. 141 mcg/l, p=NS). 3) Lower iodine excretion in women
    with cancer, regardless of menopausal status.
    In order to control for halide effect, urinary bromide level was determined in a subset of
    these women (n=47). Urinary bromide levels trended towards higher excretion by 64% in
    women without cancer (18.5 mg/l vs. 11.3 mg/l, p=NS), in premenopausal women by
    36% (20.5 mg/l vs. 15.1mg/l, p=NS), and smokers by 35% (22.7 mg/l vs. 16.8 mg/l,
    Discussion:  These preliminary results are the first to show a significant decrease in
    iodine excretion in women with malignant breast diseases.  Basic studies have shown
    a significantly lower iodine availability in breast tissue harboring malignancy.  These
    data indicate that iodine plays a role in breast cell differentiation.  These provocative
    findings imply potential diagnostic and therapeutic capabilities in the iodine pathway.

  • A 2006 Breast Cancer Patient-Iodine Study
    Finds Patients Low in Iodine, High in theToxins Bromine and Fluoride

    Brownstein, D., Iodine.  Why You Need It, Why You Can't Live Without It, 2nd Edition,
    Medical Alternatives' Press 2006.

    Editor's Note: Dr. David Brownstein, using the iodine-loading test, conducted a very
    small study in his practice to determine the iodine, bromine, and fluoride levels in eight
    breast cancer patients and ten non-breast cancer patients.  Results:  The iodine levels
    were low in all of the patients.  Just as the levels of the toxin, bromide,  trended higher in
    the breast cancer patients in the Eskin study cited above, in this study,  the bromide
    levels similarly were significantly elevated in  the breast cancer patients as opposed to
    the non-breast cancer patients.  Also, the levels of the toxin, fluoride, were higher in the
    breast cancer patients.  Supplementing with iodine will rectify the iodine deficiency and
    importantly help the body detox these toxins.

  • Continuous Administration of Iodine to Rats Results in Strong and Persistent
    Reduction of Incidence of  Breast Tumors

    Editor's Note:  In this 2005 study, the continuous treatment of rats with iodine exhibited a
    potent protective effect (70%) on breast tumors induced by the carcinogen, MNU.  This
    effect is exerted by iodine, but not by iodide or T4.  Any interruption of the iodine
    treatment resulted in an increased incidence of tumors.The suppression by iodine
    treatment is accompanied by the development of latent tumors that do not progress to
    overt cancers, suggesting that the mechanism of action is at the promotional level,  and
    the protective mechanisms may involve regulating the oxidative environment.

    Mol Cell Endocrinol. 2005 May 31;236(1-2):49-57. Epub 2005 Apr 13.
    Inhibition of N-methyl-N-nitrosourea-induced mammary carcinogenesis by molecular
    iodine (I2) but not by iodide (I-) treatment Evidence that I2 prevents cancer promotion.
    by Garcia-Solis P, Alfaro Y, Anguiano B, Delgado G, Guzman RC, Nandi S, Diaz-Munoz
    M, Vazquez-Martinez O, Aceves C.
    Instituto de Neurobiologia, Universidad Nacional Autonoma de Mexico, Km 15 Carretera
    Qro-SLP, Juriquilla, Queretaro 76230, Mexico.

    We analyzed the effect of molecular iodine (I2), potassium iodide (KI) and a subclinical
    concentration of thyroxine (T4) on the induction and promotion of mammary cancer
    induced by N-methyl-N-nitrosourea. Virgin Sprague-Dawley rats received short or
    continuous treatment. Continuous I2 treated rats exhibited a strong and persistent
    reduction in mammary cancer incidence (30%) compared to controls (72.7%).
    Interruption of short or long term treatments resulted in a higher incidence in mammary
    cancer compared to the control groups. The protective effect of I2 was correlated with the
    highest expression of the I-/Cl- transporter pendrin and with the lowest levels of
    lipoperoxidation expression in mammary glands. Triiodothyronine serum levels and
    Na+/I- symporter, lactoperoxidase, or p53 expression did not show any changes. In
    conclusion continuous I2 treatment has a potent antineoplastic effect on the
    progression of mammary cancer and its effect may be related to a decrease in the
    oxidative cell environment.

  • Iodine, with Added Progesterone, Has a Stronger Effect Than Iodine Alone on
    Breast Tumors in Rats

    Editor's Note: Adding iodine to chemically-induced (DMBA) rat breast tumors had a
    suppressive effect on the growth of tumors. Adding iodine plus medroxyprogesterone
    (progesterone) gave the highest level of response.  The growth-suppressed tumors
    showed 100% times the iodine content than the full blown (nonsuppressed) tumors.

    J Surg Oncol. 1996 Mar;61(3):209-13. Related Articles, Links  
    Suppressive effect of iodine on DMBA-induced breast tumor growth in the rat
    by Funahashi H, Imai T, Tanaka Y, Tobinaga J, Wada M, Morita T, Yamada F, Tsukamura
    K, Oiwa M, Kikumori T, Narita T, Takagi H.
    Department of Surgery II, Nagoya University School of Medicine, Japan.

    Concerning the suppressive effect of inorganic iodine on the growth of 7,12-dimethyl-
    benz(a)anthracene (DMBA)-induced breast tumor in female Sprague-Dawley (SD) rats,
    we previously reported that although iodine itself had a suppressive effect on the tumor
    growth, its effect was not as strong as that of MPA (medroxy-progesterone acetate).
    However, the combined medication of iodine at a low concentration + MPA showed a
    stronger effect than MPA alone. The purpose of the present study is to elucidate this
    mechanism of action by determining the uptake of the administered iodine into breast
    tumor tissue. Breast tumors were induced with DMBA in female SD rats, and these
    animals were treated with MPA + inorganic iodine at various concentrations for 4 weeks
    to determine tumor growth and tumor iodine content. In the comparison of tissue iodine
    content in growth-suppressive tumors with that in nonsuppressive tumors, the former
    showed a much higher iodine content. This suggests that direct uptake of inorganic
    iodine by breast tumors led to the suppression of tumor growth.

  • Seaweed's Anti-Cancer Effect on Rats

    Editor's Note:  Rats fed 5% Laminaria, a brown seaweed, then given the carcinogen,
    DMBA, had a delayed time to the occurrence of tumors and fewer adenocarcinomas.

    Cancer Res. 1984 Jul;44(7):2758-61
    Dietary seaweed (Laminaria) and mammary carcinogenesis in rats
    by Teas J, Harbison ML, Gelman RS.

    To test the potential in vivo antitumor effect of dietary seaweed, we induced mammary
    tumors in female Sprague-Dawley rats with the carcinogen 7,12-dimethylbenz(a)
    anthracene. Twenty-one-day-old rats (n = 108) were divided into two groups. Controls
    were fed a standard semipurified diet, and experimental rats received the control diet
    with 5% Laminaria, a brown seaweed, replacing 5% alphacel . At 55 days of age, each
    rat received 5 mg 7,12-dimethylbenz(a)anthracene intragastrically. Rats were palpated
    for mammary tumors and weighed weekly for 26 weeks. Complete autopsies were then
    done on all rats. The seaweed diet did not alter weight gain or weights of body organs at
    autopsy. Experimental rats had a significant delay in the time to tumor (p = 0.007);
    median time until tumor was 19 weeks in experimental rats and 11 weeks in control
    animals. Among mammary adenocarcinoma tumor-bearing animals, experimental rats
    had fewer adenocarcinomas/individual (p less than 0.05). There was also an overall
    13% reduction in the number of experimental rats with histologically confirmed
    adenocarcinomas (76% among the control rats compared to 63% among the
    experimental rats). Components of Laminaria which might account for the observed
    difference in mammary tumor growth are varied and include the sulfated polysaccharide
    fucoidan . Rats in the top row of cages had a significant (p = 0.01) delay in time to tumor
    compared to rats in the lower four rows. In each row, the seaweed-fed rats had a longer
    time to tumor than did the control rats.

  • Iodine-Rich Seaweed Exhibits an Anti-cancer Effec on Rats Fed 1.0% and 5.0%
    Wakame Seaweed

    Editor's Note: When rats were fed lesser amounts of seaweed,1.0% and 5.0% of wakame
    seaweed, then given the carcinogen, DMBA, there was  similarly a significant
    suppression of tumor growth and delay to the time of tumor occurrence.

    Jpn J Cancer Res. 1999 Sep;90(9):922-7.
    Wakame seaweed suppresses the proliferation of 7,12-dimethylbenz(a)-anthracene-
    induced mammary tumors in rats.

    by Funahashi H, Imai T, Tanaka Y, Tsukamura K, Hayakawa Y, Kikumori T, Mase T, Itoh
    T, Nishikawa M, Hayashi H, Shibata A, Hibi Y, Takahashi M, Narita T.
    Department of Surgery II, Nagoya University School of Medicine.

    We examined the anti-tumor proliferation effects of wakame seaweed on 7,12-
    dimethylbenz(a)-anthracene (DMBA)-induced rat mammary tumor. DMBA was
    administered to 8-week-old female Sprague-Dawley rats, and rats which developed
    mammary tumors were assigned randomly to three groups. Commercial rat feed was
    used in a control group (group I-A), and two feed mixtures were prepared, which
    contained commercial rat feed blended with wakame at 1.0% (group I-B) and 5.0%
    (group I-C) by weight. The respective feeds were given to each group for 8 weeks, and
    changes in mammary tumor size were compared. At the end of the experiment,
    mammary tumors and thyroid glands were resected to compare their weights. Serum
    total iodine and thyroxin (T4) levels were measured. Immunohistochemical studies for
    bromodeoxyuridine (BrdU) labeling, transforming growth factor (TGF)-beta, and
    apoptosis were carried out in the resected tumor. Significant suppression of tumor
    growth was observed in groups I-B and I-C compared with I-A. In groups I-B and I-C, the
    weights of resected mammary tumors were significantly lower and serum total iodine
    concentration was significantly higher than in I-A. BrdU indices were significantly lower
    in groups I-B and I-C, compared with I-A. TGF-beta and apoptotic index were inversely
    related to BrdU. These results suggest that iodine is transported from the serum into
    mammary tissues and induces apoptosis through the expression of TGF-beta. In
    conclusion, wakame suppressed the proliferation of DMBA-induced mammary tumors.
    seaweed-fed rats had a longer time to tumor than did the control rats.

  • Seaweed's Anti-Cancer Effect on Human Breast Cancer Cells Iodine-Rich
    Mekabu Seaweed Exhibits an Anti-cancer Effect In the Lab on Human Breast
    Cancer Cells

    Editor's Note: In the lab, mekabu, which is a part of the wakame seaweed plant, induced
    cell death in three kinds of human breast cancer cells.  Mekabu had a more potent effect
    on the cancer cells than the chemo drug, 5-fluorouracil, that is used to treat breast
    cancer.  The researchers speculated that "seaweed may be applicable for prevention of
    breast cancer".

    Jpn J Cancer Res. 2001 May;92(5):483-7.
    Seaweed prevents breast cancer?
    by Funahashi H, Imai T, Mase T, Sekiya M, Yokoi K, Hayashi H, Shibata A, Hayashi T,
    Nishikawa M, Suda N, Hibi Y, Mizuno Y, Tsukamura K, Hayakawa A, Tanuma S.
    Department of Surgery II, Nagoya University School of Medicine, Showa-ku, Nagoya 466-
    8550, Japan.

    To investigate the chemopreventive effects of seaweed on breast cancer, we have been
    studying the relationship between iodine and breast cancer. We found earlier that the
    seaweed, wakame, showed a suppressive effect on the proliferation of DMBA
    (dimethylbenz(a)anthracene)-induced rat mammary tumors, possibly via apoptosis
    induction. In the present study, powdered mekabu was placed in distilled water, and left
    to stand for 24 h at 4 degrees C. The filtered supernatant was used as mekabu solution.
    It showed an extremely strong suppressive effect on rat mammary carcinogenesis when
    used in daily drinking water, without toxicity. In vitro, mekabu solution strongly induced
    apoptosis in 3 kinds of human breast cancer cells. These effects were stronger than
    those of a chemotherapeutic agent widely used to treat human breast cancer.
    Furthermore, no apoptosis induction was observed in normal human mammary cells. In
    Japan, mekabu is widely consumed as a safe, inexpensive food. Our results suggest
    that mekabu has potential for chemoprevention of human breast cancer.

  • Iodine as a cancer-seeking missile. Possible future in
    diagnosis and treatment.

    Med Hypotheses. 2013 Jan;80(1):94-8. doi: 10.1016/j.mehy.2012.10.018. Epub 2012
    Nov 19.
    The potential of iodine for improving breast cancer diagnosis and treatment.
    Altman MB, Flynn MJ, Nishikawa RM, Chetty IJ, Barton KN, Movsas B, Kim JH, Brown SL.
    Source. Henry Ford Health System, Department of Radiation Oncology, 2799 W. Grand
    Blvd., Detroit, MI 48202, USA.

    Early detection through modalities such as mammography remains pivotal in the fight
    against breast cancer. The detectability of breast cancer through mammography is
    rooted in the differential X-ray attenuation properties of cancerous and normal breast
    tissue. An unexplored component of the X-ray contrast between fibrous breast tissue
    and similarly composed tumor tissue is the presence of naturally localized iodine in the
    cancer but not healthy breast tissue. It is hypothesized that differing amounts of iodine
    are present in tumor versus normal breast tissue that leads to more easily detectable
    cancer due to an increased Z value of the tumor tissue relative to the healthy tissue,
    which results in enhanced differences in X-ray attenuation properties between the two
    tissues and thus greater radiographic contrast. The hypothesis is supported by
    experimental observations explaining how iodine could localize in the tumor tissue but
    not surrounding healthy tissue. Breast cancer cells express the sodium-iodide
    symporter (NIS), an ion pump which sequesters iodine in tumor cells. Healthy non-
    lactating breast tissue, in contrast, does not express NIS. Further evidence for the
    differential expression of NIS resulting in X-ray contrast enhancement in breast cancer is
    the established correlation between expression of insulin growth factor (IGF) and
    enhanced X-ray contrast, and the evidence that IGF is a promoter for NIS. Ultimately, if
    the expression of iodine can be shown to be a component of radiographic contrast
    between healthy and tumor breast tissue, this could be used to drive the development of
    new technology and techniques for use in the detection and treatment of breast cancer.
    The proof of this hypothesis could thus have a substantial impact in the fight against
    breast cancer.

  • Iodine + Selenium:  Selenium is Needed For Proper Functioning of Iodine

    Editor's Note:  Deiodinase enzymes which convert T4 (thyroxine, the prohormone that
    has four atoms of iodine ) into T3 (triiodothyronine, the cellularly active hormone that has
    three atoms of iodine), and then convert T3 into T2 are selenium-dependent.  In addition
    to being incorporated into thyroid hormones, iodine is organified into anti-proliferative
    iodilipids in the thyroid;  such compounds may play a role in the proliferative control of
    other tissues, such as the breast.  Selenium acts synergistically with iodine.  Thus,
    selenium may affect hormone homeostasis and iodine availability.  

    Cancer Causes Control. 2000 Feb;11(2):121-7.
    Hypothesis: iodine, selenium and the development of breast cancer.
    Cann SA, van Netten JP, van Netten C.
    Special Development Laboratory, Royal Jubilee Hospital, Victoria, BC, Canada.

    BACKGROUND: In this paper we examine some of the evidence linking iodine and
    selenium to breast cancer development. Seaweed is a popular dietary component in
    Japan and a rich source of both of these essential elements. We hypothesize that this
    dietary preference may be associated with the low incidence of benign and malignant
    breast disease in Japanese women. In animal and human studies, iodine
    administration has been shown to cause regression of both iodine-deficient goiter and
    benign pathological breast tissue. Iodine, in addition to its incorporation into thyroid
    hormones, is organified into anti-proliferative iodolipids in the thyroid; such compounds
    may also play a role in the proliferative control of extrathyroidal tissues. Selenium acts
    synergistically with iodine. All three mono-deiodinase enzymes are selenium-dependent
    and are involved in thyroid hormone regulation. In this way selenium status may affect
    both thyroid hormone homeostasis and iodine availability. CONCLUSION: Although
    there is suggestive evidence for a preventive role for iodine and selenium in breast
    cancer, rigorous retrospective and prospective studies are needed to confirm this

  • Taking Vitamin C with Iodine

    Vitamin C:  Using Nutrition to Improve Iodine Transport Defect To Help Iodine Enter
    Abraham GE and Brownstein D., Evidence that the Administration of Vitamin C Improves
    a Defective Cellular Transport Mechanism for Iodine: A Case Report, The Original
    Internist 2005.

    (There is no abstract available.  To read the entire study, go to: http://www.optimox.

    Editor's Summary:
    Drs. Abraham and Brownstein describe a case of using nutrition - vitamin C and chloride
    - to improve the function of a defective iodine cellular transport system to help iodine
    enter cells. To help enable iodine to be absorbed by the cells, two iodine transport
    systems, the sodium/iodide system (NIS) - one atom of iodine is transported into cells
    and two atoms of sodium are transported out of cells,  and the chloridide/iodide (pendrin)
    system help facilitate the transportation of iodine into cells.  Rarely, these iodine cellular
    transport systems can become blocked or damaged, leaving cells iodine-deficient.  In
    this case report, on an iodine-loading test, a woman excreted 90% of the iodine, which
    usually implies iodine sufficiency, but the high excretion rate was coupled with a low
    serum inorganic iodide level, suggesting  a defect in the iodine retention mechanism.  
    She also had elevated levels of bromide - a toxic halide - in her urine and serum.  The
    elevated bromide may have caused oxidative damage to the iodine transport system.
    Since chloride competes with bromide and increases the elimination of bromide,
    chloride was administered at 10mg/day for one week.  The result:  A marked increase in
    bromide excretion.  Plus, she was given the antioxidant vitamin C at 3gm/day for three
    months. At the end of three months of nutrititonal support, she increased her baseline
    serum inorganic iodide level, and her retention of  iodine was increased from 10% to
    50%.  This case report presents evidence of nutrition  helping to improve the function of
    the iodine cellular transport mechanism.

    IODINE AND BREAST CANCER SUMMARY:  Does Iodine Act as an Anti-Estrogen, Like  
    the Drugs, Arimidex and Tamoxifen?

    From Eskin BA's study,  Iodine and Mammary Cancer, cited in the IODINE and BENIGN
    BREAST DISEASE section, iodine is stated to be a requisite element for normal breast
    tissue.  Iodine deficient tissues show changes in, among other things, estrogen
    receptor proteins.  Supplementing with iodine would make the breast tissue less
    susceptible to stimulation from excess estrogen, which is produced by the ovaries in an
    iodine-deficient state and courses through the blood. Thus, iodine acts as an anti-

    Arachidonic acid (polyunsaturated fats) and its metabolites, COX and LOX, exert a
    dedifferentiative effect on breast tissue.  "PGE2, as a product of cyclooxygenase (COX),
    stimulates the gene expression of aromatase in the fatty tissue of the breast, whereby
    intramammary estrogen increases". (Torremante P., Mastopathy, Breast Cancer and
    Iodolactones, cited in the IODINE'S  MECHANISMS of ANTI-TUMOR ACTION section.)
    Plus, in the Hartmann et al. study in the IODINE and BENIGN BREAST DISEASE section,
    the 41 out of 235 women who had atypia who went on to develop breast cancer, had
    significantly higher levels of COX-2 or cyclooxygenase-2, the enzyme produced in the
    body when there is inflammation and which is also produced in precancerous tissues.

    When arachidonic acid becomes iodinated (bound to iodine), the iodolactones that are
    formed inhibit the EGF (epidermal growth factor) receptor, whereby the metabolism of
    arachidonic acid induced by EGF and TGFa (powerful growth factors) is inhibited.

    Thus, powerful arguments can be made that iodine may be a de facto anti-estrogen and
    aromatase inhibitor in the manner of the drugs, Arimidex and Tamoxifen.

  • Calling for Iodine to be Considered as an Adjuvant Therapy for Breast Cancer

    Carmen Aceves,  in her review article,  Is Iodine a Gatekeeper of the Integrity of the
    Mammary Gland?, cited in the IODINE'S MECHANISMS of ANTI-TUMOR ACTION section,
    states,  "We propose that  an I2 (iodine) supplement should be considered as an
    adjuvant in breast cancer therapy."

References: What is the effect of iodine on breast cancer?