Breast Cancer Choices
|Scrutinizing the evidence for breast
cancer procedures and treatments
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.
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.
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.
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.
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.
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. firstname.lastname@example.org.
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.
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
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-
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.
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
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
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
(There is no abstract available. To read the entire study, go to: http://www.optimox.
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.
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?