HomeMy WebLinkAboutCOM 0392.001 2014-2016 Margaret Wille t+of- Phone No. Hilo: (808)961-8027
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Council Member <P.• +, Phone No. Waimea: (808)887-2043
District 9-North and South Kohala " ����' Fax No.: (808)887-2072
;I' ' ' • ' E-Mail: mwille@co.hawaii.hi.us
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HAWAII COUNTY COUNCIL
County of Hawai`i
Hawai'i County Building Holomua Center West Hawaii Civic Center Bldg.A
25 Aupuni Street 64-1067 Mamalahoa Highway, Suite C-5 74-5044 Ane Keohokalole Hwy.
Hilo, Hawaii 96720 Waimea, Hawaii 96743 Kailua-Kona, Hawaii,96740
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TO: Dru Mamo Kanuha, Council Chair
And Members of the Hawai`i C.u s ty Council cp =
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FROM: f Margaret Wille, Council Me r I 4 ' .
DATE: August 4, 2015 I
SUBJECT: Additional Information for Bill No. 71
Please find attached additional information from Dr. McGaff for reference during the
Bill No. 71 discussion on August 4, 2015.
Thank you.
MW/dh
att
Comm. No. 3Qa . I
Ref. To: f art C....-
Serving the Interests of the People of Our Island Rif Date AU 1 a
Hawai`i County Is An Equal Opportunity Provider And Employer
Food Chem Toxicol. 2013 Sep;59:129-36. doi: 10.1016/j.fct.2013.05.057. Epub 2013 Jun
10.
Glyphosate induces human breast cancer
cells growth via estrogen receptors.
Thongprakaisang S�,Thiantanawat A, Rangkadilok N, Suriyo T,Satvavivad J.
Author information
Abstract
Glyphosate is an active ingredient of the most widely used herbicide and it is believed to
be less toxic than other pesticides. However,several recent studies showed its potential
adverse health effects to humans as it may be an endocrine disruptor. This study focuses
on the effects of pure glyphosate on estrogen receptors(ERs)mediated transcriptional
activity and their expressions. Glyphosate exerted proliferative effects only in human
hormone-dependent breast cancer,T47D cells, but not in hormone-independent breast
cancer, MDA-MB231 cells, at 100 12 to 100 OM in estrogen withdrawal condition, The
proliferative concentrations of glyphosate that induced the activation of estrogen response
element(ERE)transcription activity were 5-13 fold of control in T47D-KBluc cells and
this activation was inhibited by an estrogen antagonist, ICI 182780, indicating that the
estrogenic activity of glyphosate was mediated via ERs. Furthermore,glyphosatezlso
altered both ERa and (3 expression. These results indicated that low and environmentally
relevant concentrations of glyphosate possessed estrogenic activity. Glyphosate-based
herbicides are widely used for soybean cultivation,and our results also found that there
was an additive estrogenic effect between glyphosate and genistein, a phytoestrogen in
soybeans. However,these additive effects of glyphosate contamination in soybeans need
further animal study.
Copyright D 2013 Elsevier Ltd. All rights reserved.
KEYWORDS:
Estrogenic effect; Genistein; Glyphosate; Human breast cancer; T47D; T47D-KBluc
New research and the TH3 epidemic—
Before we dive into the reasoning behind why we are seeing so many TH3
thermograms, let's review the physiology that causes these infrared images.
Estrogen is a powerful steroid that, in the breast, primarily acts upon the ductal
cells. The hormone causes the ductal cells to grow and multiply. Normal levels of
estrogen (estrogen in balance with progesterone) cause normal ductal cell
changes. Unopposed estrogen (lack of balance resulting in increased levels of
estrogen) causes an increase in ductal cell growth and multiplication (ductal
hyperplasia). This stimulation of the ductal cells causes an increase in cellular
metabolism. In order to sustain this cellular growth and multiplication, the cells
demand more oxygen and metabolites (food). This causes an increase in the
size and number of blood vessels in order to bring in nutrients and remove
waste. The end result is an infrared image that has a symmetrical appearance of
a specific vascular pattern originating from the main arterial supply and venous
drainage of the breast.
Estrogen plays a major role in the pathogenesis of breast cancer via the uptake
into the cell through the mechanism of the estrogen receptor(ER). Its association
with many of the epidemiological risk factors for breast carcinoma (e.g. age of
menarche, first child, breast feeding, menopause, and the use of oral
contraceptives, or hormone replacement therapy) is well known. The
pathogenesis of estrogen as it relates to the cause of breast cancer is through
two mechanisms: 1.) The aromatization (breakdown) of estrogen in the breast
causing carcinogenic byproducts and, 2.) Direct stimulation of pre-cancerous and
cancerous cellular growth (cancerous ductal cells).
Some studies suggest that the use of soy and flax will block the ER, thus
decreasing the risk of breast cancer. Unfortunately, if the key (estrogen, soy, flax,
etc.) fits the lock (ER receptor on the cell membrane) it may open the door to the
effects on the cell. How would we know if the ER was either blocked or
triggered? Perhaps we can observe the effects via MIR. It is well established that
the effects of various hormones on the breast can be detected by MIR. The
infrared vascular display produced by increased levels of estrogen, the hormones
of pregnancy, and the hormonal interactions during lactation are well established
and understood. When unopposed estrogen is treated, and hormonal balance is
restored in the breast, the infrared display is returned to normal. We see this
same effect when breast cancer patients are given Tamoxifen. More than 75% of
all breast cancers are ER positive. This means that in these patients estrogen
promotes the growth of their cancer. Tamoxifen is classified as an ER antagonist,
it blocks the receptor so that circulating estrogen cannot bind and activate the
cancer cells. VVhen comparing the initial breast cancer images of these patients
to the post-surgical images we not only see the resolution of the malignant
neoangiogensis, but the background evidence of estrogen dominance has also
resolved due to the patient taking Tamoxifen. We also have evidence of many
variations on this theme (e.g. post-surgical images before Tamoxifen use) still
resulting in the normalization of the estrogen dominant images due to Tamoxifen.
Now that we have established that MIR has the ability to detect the effects of
unopposed estrogen, and the positive effects of treatment (e.g progesterone,
Tamoxifen), how does this relate to phytoestrogens and xenoestrogens?
If, as it has been postulated, soy and other phytoestrogens such as flax act as
ER receptor blockers, we should be able to clearly observe these effects with
MIR. Unfortunately, what we observe in the vast majority of women is the
opposite. Soy and flax, but soy to a much great extent, affects the breast in the
same way as estrogen. And again, how do we know this? When women take
these phytoestrogens their MIR images change from normal to the vascular
pattern seen with unopposed estrogen; and when they stop taking theses
phytoestrogens their images return to normal. What this is demonstrating is that
these phytoestrogens are binding with the ER and causing the same direct ductal
cell stimulation, and resulting increase in vascularity, that estrogen does. Many
women who stop taking soy will also tell you that their breasts become less sore,
tender, and fibrocystic to the touch. This is also one of the same things women
will tell you when stopping medications that left them estrogen imbalanced.
Studies on phytoestrogens, especially on soy, also support these findings. ft is
unfortunate that the media, and the soy boards, push only the studies that
promote things their way.
Now that we have a handle on how the physiology of the breast is affected, and
how this affects the MIR images, let's discuss what this has led to over time.
Some of you may have been noticing that over the past few years there has been
a definite rise in the number of breast images that are being graded as TH3s.
Along with this has been a steady decrease in TH 1 s. This has also been
observed by other thermologists. We have been discussing the possible reasons
for this and have put forth a plausible reason. A steady increase in use of soy in
the diet, along with xenoestrogens and the increased use of flax seed products,
is causing two things to occur in the breast: 1.) Direct stimulation of ductal cell
growth and multiplication, and, 2.)A "fertile field" of open vasculature in the
breast as a byproduct of the effects of these"other" estrogens on the metabolism
of the ductal cells. In this environment, atypical cells (pre-cancer), early stage
DCIS, or other breast cancers may receive direct stimulation promoting growth
(e.g. ER positive cancers) along with taking advantage of the resulting increase
in blood flow to maintain growth. This, in turn, may be creating the vascular
asymmetries and hyperthermic findings we are seeing in all these TH3s.
Phytoestrogens in the diet, primarily soy, has increased at an alarming rate. It is
becoming very difficult to find foods that do not contain soy. As such, the public is
being forced to eat ever increasing amounts of soy without their knowledge.
Taking this into consideration, and adding deliberate uses of soy in the diet (tofu,
soy milk, etc.), may be causing the increased number of TH3 gradings via the
pathway mentioned above. To this can be added xenoestrogens found in make-
up, shampoo, sunscreens, and many other hygiene products and chemicals in
our home and office environments. Considering these exposures as a whole
could account for the significant rise in estrogen dominant images seen over the
past 15 years. In 1995 we used to see approximately 45-50% of women scanned
with estrogen dominant images; the number now approaches 95%. The resulting
direct stimulation of cellular growth, and increase in blood flow, may be pushing
more and more thermograms into the TH3 range.
A new piece of the puzzle is also emerging. I recommend that you do a search
on the net for GMO (genetically modified) foods and pesticides. There is brand
new research out showing strong evidence that GMO foods, especially combined
with common pesticides, causes cancer. Due to these findings a great number of
countries around the world are now refusing to purchase GMO crops from other
countries. They are taking this very seriously.
Many of the pesticides alone have been found to have powerful estrogenic
effects. And even more data is coming out about certain regions using powerful
herbicides to kill plants encroaching on roadsides. These pesticides and
herbicides are very powerful xenoestrogens; so much so that the sex of fish,
alligators, and other aquatic animals are being altered to female when rain runoff
takes these pesticides and herbicides into lakes. These are powerful endocrine
disrupters.
Add these new xenoestrogen findings to the known dietary intake of soy and we
have a recipe for an epidemic of TH3s (See the paper published below. This is
only one example of many papers on this subject). The breast is being
bombarded by so many outside estrogen sources that it makes sense that we
are seeing what we are seeing. Keep in mind that these xenoestrogens have an
affinity for fat tissue and can build up in the fat tissue over time. I now understand
why so many women over 50 are showing thermograms that have the vascular
appearance of pregnancy, and sometimes lactation!
As a warning signal, these TH3 images may be considered the best news for
women. These women now have a chance to make changes and possibly head
off a future cancer at a point in time that is extremely early. We have the
technology to warn women of this situation and alert their doctors to this problem.
I truly believe that we have the finest technology available at this time to play the
most important role in prevention.
Isn't it incredible, we were seeing all of these metabolic breast changes long
before the possible causes were found. Thermography is the proverbial canary in
the mine!
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Data trends show correlation between increase in organ disease and GMOs - Seattle GMO I Examiner.com Page 3 of 5
Correlation does not necessarily imply cause and there may be other factors. Other known endocrine
disruptors are: BPA (bisphenol-A) & phthalates (both in plastics), dioxins (byproduct of smelting,
paper bleaching, manufacture of herbicides and pesticides), and atrazine polychlorinated biphenyls
(PCBs -- used in electrical equipment, coatings, inks, adhesives, flame-retardants, and paints).
Indeed, we are bombarded with a veritable cocktail of chemicals daily in addition to GMOs and their
associated herbicides. These include food preservatives (BHA & BHT), water contaminants (chlorine
& fluoride), food additives (aspartame, monosodium glutamate, carrageenan), and food coloring to
name a few. We have been exposed to an increasing background level of chemicals for over 40
years. The body burden becomes overwhelming. GMOs may be pushing us off the cliff. Certainly
more research should be done to firmly establish causality.
Acknowledgment: Jon Abrahamson helped with data mining for this article.
Notes:
There are many scientific studies showing that glyphosate and the additives in Roundup are toxic to
human cells. Below is a list of those most pertinent to this discussion.
In 2004, Marc et al. reported that glyphosate-based pesticides cause cell-cycle dysfunction that leads
to development of cancer.
In 2009 Cashier et al. published an article in the journal Toxicology citing evidence that glyphosate-
based (G-based) herbicides are endocrine disruptors in human cells. They reported toxic effects to
liver cells "at 5 ppm [parts per million], and the first endocrine disrupting actions at 0.5 ppm, which is
800 times lower than the level authorized in some food or feed (400 ppm, USEPA, 1998). ... In
conclusion, according to these data and the literature, G-based herbicides present DNA damages ...
on human cells."
In 2012 Koller et al. reported that glyphosate and its formulation (Roundup) is toxic to cells,
particularly organ cells, and exhibits DNA-damaging properties "after short exposure to
concentrations that correspond to a 450-fold dilution of spraying used in agriculture."
What is often overlooked is the role of"inert" ingredients in glyphosate formulations like Roundup,
which have been found to amplify glyphosate toxicity.
In 2005, Richard et al. reported that "glyphosate is toxic to human placental JEG3 cells within 18 hr
with concentrations lower than those found with agricultural use, and this effect increases with
http://www.examiner.com/article/data-trends-show-correlation-between-increase-organ-disease-and-gmos 9/21/2013
Data trends show correlation between increase in organ disease and GMOs - Seattle GMO I Examiner.com Page 4 of 5
concentration and time or in the presence of Roundup adjuvants. Surprisingly, Roundup is always
more toxic than its active ingredient. ... We conclude that endocrine and toxic effects of Roundup, not
just glyphosate, can be observed in mammals."
In 2012, Mesnage et al. reported, "This study demonstrates that all the glyphosate-based herbicides
tested are more toxic than glyphosate alone The formulated herbicides (including Roundup) can
affect all living cells, especially human cells. Among them, POE-15 clearly appears to be the most
toxic principle against human cells, ... We demonstrate in addition that POE-15 induces necrosis
when its first micellization process occurs, by contrast to glyphosate which is known to promote
endocrine disrupting effects after entering cells."
Data Sources:
Diabetes incidence data: CDC
Diabetes prevalence data: CDC
ESRD data: U.S. Renal Data System
Blood pressure data: CDC
Obesity data: CDC
Acute Kidney Injury: National Kidney and Urologic Diseases Information Clearinghouse
(NKUDIC) a service of NIH.
Cancer data: National Cancer Institute-Surveillance Epidemiology and End Results (SEER).
SEER 9 areas (San Francisco, Connecticut, Detroit, Hawaii, Iowa, New Mexico, Seattle, Utah, and
Atlanta). Rates are per 100,000 and are age-adjusted to the 2000 US Std Population (19 age groups
- Census P25-1130).
Glyphosate: USDA:NASS National Agricultural Statistics Service (NASS)
Percent GE corn & soy crop data:
1996-1999: USDA Agricultural Economic Report No. (AER-810) 67 pp, May 2002
2000-2012: USDA:NASS National Agricultural Statistics Service
http://www.examiner.com/article/data-trends-show-correlation-between-increase-organ-disease-and-gmos 9/21/2013
Number of People Diagnosed with Diabetes in U.S. (prevalence)
O Persons yviDiabetes plotted against glyphosate applied to corn &soy crops
—%GE soy S.corn crops along with percentage of GE corn&soy grown in US.
--.Glyphosate apphed to
Corn&Soy Pearson's coefficients for glyphosate and prevalence
R=0.9819-8,p<= 4.44e-09
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....Glyphosate applied to Corn
soy along with glyphosate applied on corn&soy in U.S
46 GE soy&corn crops Pearson's coefficients for glyphosate &incidence
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•male&female Thyroid Cancer Incidence Rate
0.0 Glypliosate applied to Corn&
Soy
Sc GE soy&corn owns plotted against amount of glyphosate applied to U S corn &soy crops
male along with the percentage of genetically engineered corn &soy crops
—terrtaie Pearson correlation coefficients for glyphosate&both male and female incidence
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---%GE soy&corn crops
male Plotted against amount of glyphosate applied to corn &soy
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Glyphosate applied to along with percentage of GE corn and soy planted in U.S.
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Corn&Soy Pearson's coefficients for glyphosate and both male&
—female female incidence: R=4.975, p <= 1.79e-08
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—Glyphosate apvoedm plotted against glyphosate applied to corn & soy
corn soy
—p^GEcorn msoy crops along with percent of GE corn & soy planted in U.S.
...ornate Pearson correlation coeficients for glyphosate and both
--female male and female incidence: R=.9578, p<= 5.14e-08
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The data for corn and soy crops have also been plotted against: % of U.S. population who are obese,
who have high blood posysure, and hospitalizations for acute kidney injury (a soddeu, temporary, and
sometimes fatal loss of kidney function). While these data aren't available before 1995, tbwtrcodo are
remarkably coincident.
oMedian%people Obesity in U.S. Population (percent)
"»°"°
~"it ss corn tt"", plotted against amount of glyphosate applied to &soy crops
—~n*v"""°m""corn& n= 0.9988. p <= 9.76e'07
soy along with percent GE ccin &soy crops planted in U.S.
R=0.3843. p <= 1250-06
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