Breast Cancer ChoicesTM |
| . |
| Scrutinizing the evidence for breast cancer procedures and treatments |
| Fluoride and Vitamin D |
| . |
Subtraction Strategy * Personal Products Dental Detox House Detox Water Detox Breast Detox Addition Strategy CoQ10 Curcumin Selenium Enzymes Melatonin Vitamin C Vitamin D Medicinal Foods |
The risk of dying of breast cancer was 73 percent higher in women with too-low levels of vitamin D versus women in the optimal range. |
Vitamin D3 is the natural human form of vitamin D made in the skin when cholesterol reacts with sunlight. with D2 which may be found in small amounts in multivitamins. |
Can Vitamin D levels be used as a breast cancer screening tool? Watch Dr. Cedric Garland's video |
Low levels of vitamin D levels such as 400- 800 units have not proven effective in many studies using Vitamin D therapeutically. |
| . |
| . |
| . |
Toronto Vitamin D Deficiency Seminar Speakers Symposium 2009 in Print click here |
| Not absorbing Vitamin D orally? Some physicians recommend Vit D injections. |
Fluoride by Aliss Terpstra
Fluoride is a toxic substance known to inhibit hundreds of enzymes
including those that generate ATP to power the cell. Fluoride also affects
the iodine transport system and thyroid hormone activation. The recent
(2006) National Research Council report on the toxicology of fluoride in
drinking water admits it is an “endocrine disruptor.”
Fluoride is greatly increased in the modern diet, added to drinking water
in nearly every North American large city, and is a large component of air
pollution, entering the blood through the lungs. Most North Americans
have excessive intake. Up to 80% of intake is retained in the body,
accumulating in skeletal tissue from conception. Fluoride is not
metabolized and is not a nutrient, but does increase the need for other
nutrients, notably calcium, iodine, selenium, C, E and possibly D.
Vitamin D3 is an essential nutrient substance and cell function regulator,
made in the skin from exposure to UVB radiation from the sun (or tanning
lights) and naturally present in some animal and sea foods. There is
emerging consensus among researchers that humans need a blood level
of 80-100 nmol/L from conception to old age for optimal growth and health
including basic protection from infection, autoimmune disease and cancer.
Most of the world’s people, all ages, now living indoors and eating
processed foods, are deficient. It is theorized that some incidence of
some cancers, including breast cancer, could be reduced by up to half
with optimization of blood D levels in the general population. However,
researchers admit that a fixed supplement dosage does not reliably
produce a corresponding optimal level of 25OHD in the blood. Some
research points to low thyroid function in cases of stubborn D deficiency.
Accuracy of blood tests for 25OHD has also been a problem.
The role of fluoride as an antagonist to reaching optimal D in the blood
has never been examined.
Does our increased fluoride intake from food, water and environmental
pollution play a role in suppressing vitamin D formation in skin, uptake
from food, synthesis and conversion in liver and kidney tissues, and
activation in cells? Does it compete with 25OHD to limit vitamin D receptor
formation, or affect metabolic degradation of calcitriol (the active
hormone-like form of D) leading to a shortage or delay? Is fluoride’s well-
known thyroid-suppressive effect part of the D-deficiency picture? Does
increased fluoride intake cause dose-related relative deficiency of
cancer-protective vitamin D as it does with iodine, selenium and
antioxidants like C and E?
Could this effect account for part of the increase in cancer incidence and
mortality reported in epidemiological and animal studies on artificially
fluoridated drinking water?
Research throughout the twentieth century found that clinical Vitamin D
deficiency disease of the bones can be caused by increased fluoride
intake: http://www.fluoridealert.org/health/bone/fluorosis/rickets.html
Increased fluoride intake also produced deficiency of the active vitamin D
metabolites (25OHD and 1,25OHD) normally produced by the liver and
kidney.
Canadian research correlated higher vitamin D blood levels (25OHD
above 100 nmol/L) with better survival odds after breast cancer
diagnosis, as well as cancer that is less aggressive. This has given new
hope that low-cost dietary supplements, D-enriched foods and sunshine
can aid in cancer prevention and improve survival after diagnosis and
treatment.
British researchers found that breast cancer cells are able to protect
themselves against vitamin D’s cancer-fighting chemistry by inhibiting
enzymes that activate it from 25OHD (calcidiol) into 1,25OHD (calcitriol) at
the cell margins. This effect was most pronounced when levels of 25OHD
outside the cell were low. The British researchers concluded that higher
levels of 25OHD outside the cell are needed in order to overcome the
cancer cell’s defense. When the cancer cell is faced with ample calcidiol,
the formation of more vitamin D receptors and activation of more calcitriol
tends to promote apoptosis and slow or even stop tumor growth.
If vitamin D is as important in fighting breast cancer as it appears to be,
and cancer cells have defenses against it, we should know if there are
environmental or dietary factors such as increased fluoride intake that
inhibit optimal D formation and activation, directly or indirectly.
Normal thyroid function is essential for normal D metabolism. Iodine and
selenium are required for normal thyroid function. According to the
National Research Council 2006 report, chronic hypothyroidism is reliably
induced with fluoride dosage from 0.01 mg/kg/day (exceeded with
consumption of fluoridated drinking water) when iodine or selenium is
deficient. Selenium deficiency can also cause hypothyroidism, and
selenium deficiency is known to increase risk of cancer incidence and
death. The body’s major detoxification pathways that protect against
cancer require selenium. Fluoride-induced thyroid suppression may be
one aspect of D deficiency despite supplementation, and may be related
to this fluoride-induced iodine and selenium deficiency.
Lastly, Vitamin D deficiency is one aspect of hypothyroidism and
autoimmune thyroid disease, which increase risk of both breast and
thyroid cancers. Supplementation with D can be therapeutic for both
hypothyroidism and autoimmune thyroid disease.
Reducing fluoride intake should therefore be considered as part of the
clinical strategy for prevention and treatment of breast cancer and thyroid
disease, and for optimization of vitamin D levels in the blood as well as
optimization of iodine and selenium intake.
References
Anticancer Res. 2006 Jul-Aug;26(4A):2573-80. Colston KW, Lowe LC, Mansi JL, Campbell MJ.
Vitamin D Status and Breast Cancer Risk
BACKGROUND: Local synthesis of 1alpha,25(OH)D3 in breast tissue may contribute to
maintenance of normal cell function and could be impaired with low circulating levels of the
precursor 25hydroxyvitamin D. The aims of this study were to: i) assess the association
between breast cancer risk and plasma 25OHD3 concentration and ii) define the significance of
expression of the 25OHD activating enzyme CYP27b1 in non-malignant and malignant models
of breast epithelial cells. MATERIALS AND METHODS: Breast cancer patients and control
women were recruited and their 25OHD levels measured by enzyme-linked immunosorbent
assay (ELISA). MRNA expression of CYP271b and the 1,25(OH)2D3 inactivating enzyme CYP24
were measured in breast cancer cell lines by RT-PCR and correlated with immunoblotting
approaches to the translated proteins. RESULTS: For women with 25OHD < 50 nM the odds
ratio for breast cancer compared with women with 25OHD > 50 nM was 3.54 (CI 1.89-6.61, p <
0.001). CYP271b and CYP24 were detected in non-malignant and malignant cell models.
Protein levels of 24OHase but not 1alphaOHase were decreased at confluence in the cell lines.
CONCLUSION: Impaired local generation of 1,25OHD3 may contribute to the development of
breast cancer.
Clinch CA. Fluoride Interactions with Iodine and Iodide: Implications for Breast Health. Fluoride
April-June 2009:42(2):75-87.
http://www.fluorideresearch.org/422/files/FJ2009_v42_n2_p00i-iii.pdf
Goodwin P. J. et al. Samuel Lunenfeld Research Institute, Toronto, ON, Canada; University of
Toronto, Toronto, ON, Canada; Sunnybrook Health Sciences Centre, Toronto, ON, Canada; St.
Michael's Hospital, Toronto, ON, Canada. Vitamin D deficiency is common at breast cancer
diagnosis and is associated with a significantly higher risk of distant recurrence and death in a
prospective cohort study of T1-3, N0-1, M0 BC.
Goodwin, P. (2009) Vitamin D in Cancer Patients: Above all, do no harm. Journal of Clinical
Oncology, Vol 27, No 13 (May 1), 2009: pp. 2117-2119
Graham, J.R., Burk, O., and Morin, P. (1987). A current restatement and continuing reappraisal
concerning demographic variables in American time-trend studies on water fluoridation and
human cancer. Proc Pennsylvania Academy of Sci. 61:138-146.
Johnson W, et al. (1979). Fluoridation and bone disease in renal patients. In: E Johansen, DR
Taves, TO Olsen, Eds. Continuing Evaluation of the Use of Fluorides. AAAS Selected
Symposium. Westview Press, Boulder, Colorado. pp. 275-293.
National Research Council. (2006). Fluoride in Drinking Water: A Scientific Review of EPA's
Standards. National Academies Press, Washington D.C.
Susheela, A.K. (2007) A Treatise on Fluorosis. Fluorosis Research and Rural Development
Foundation. Delhi, India.
Taylor A., Taylor N. (1965). Effects of Fluoride on Tumor Growth. Proceedings of Society of
Experimental Biol. and Medicine, Vol. 65 pp252-255.
Yiamouyiannis JA. (1993). Fluoridation and cancer: the biology and epidemiology of bone and
oral cancer related to fluoridation. Fluoride. 26(2):83-96. Full study at http://www.fluoridealert.
org/re/yiamouyiannis-1993.pdf
Yiamouyiannis J., Burk D. (1977) Fluoridation and cancer age-dependence of cancer mortality
related to artificial fluoridation, Fluoride 10: 102-124.
****
Fluoride is a toxic substance known to inhibit hundreds of enzymes
including those that generate ATP to power the cell. Fluoride also affects
the iodine transport system and thyroid hormone activation. The recent
(2006) National Research Council report on the toxicology of fluoride in
drinking water admits it is an “endocrine disruptor.”
Fluoride is greatly increased in the modern diet, added to drinking water
in nearly every North American large city, and is a large component of air
pollution, entering the blood through the lungs. Most North Americans
have excessive intake. Up to 80% of intake is retained in the body,
accumulating in skeletal tissue from conception. Fluoride is not
metabolized and is not a nutrient, but does increase the need for other
nutrients, notably calcium, iodine, selenium, C, E and possibly D.
Vitamin D3 is an essential nutrient substance and cell function regulator,
made in the skin from exposure to UVB radiation from the sun (or tanning
lights) and naturally present in some animal and sea foods. There is
emerging consensus among researchers that humans need a blood level
of 80-100 nmol/L from conception to old age for optimal growth and health
including basic protection from infection, autoimmune disease and cancer.
Most of the world’s people, all ages, now living indoors and eating
processed foods, are deficient. It is theorized that some incidence of
some cancers, including breast cancer, could be reduced by up to half
with optimization of blood D levels in the general population. However,
researchers admit that a fixed supplement dosage does not reliably
produce a corresponding optimal level of 25OHD in the blood. Some
research points to low thyroid function in cases of stubborn D deficiency.
Accuracy of blood tests for 25OHD has also been a problem.
The role of fluoride as an antagonist to reaching optimal D in the blood
has never been examined.
Does our increased fluoride intake from food, water and environmental
pollution play a role in suppressing vitamin D formation in skin, uptake
from food, synthesis and conversion in liver and kidney tissues, and
activation in cells? Does it compete with 25OHD to limit vitamin D receptor
formation, or affect metabolic degradation of calcitriol (the active
hormone-like form of D) leading to a shortage or delay? Is fluoride’s well-
known thyroid-suppressive effect part of the D-deficiency picture? Does
increased fluoride intake cause dose-related relative deficiency of
cancer-protective vitamin D as it does with iodine, selenium and
antioxidants like C and E?
Could this effect account for part of the increase in cancer incidence and
mortality reported in epidemiological and animal studies on artificially
fluoridated drinking water?
Research throughout the twentieth century found that clinical Vitamin D
deficiency disease of the bones can be caused by increased fluoride
intake: http://www.fluoridealert.org/health/bone/fluorosis/rickets.html
Increased fluoride intake also produced deficiency of the active vitamin D
metabolites (25OHD and 1,25OHD) normally produced by the liver and
kidney.
Canadian research correlated higher vitamin D blood levels (25OHD
above 100 nmol/L) with better survival odds after breast cancer
diagnosis, as well as cancer that is less aggressive. This has given new
hope that low-cost dietary supplements, D-enriched foods and sunshine
can aid in cancer prevention and improve survival after diagnosis and
treatment.
British researchers found that breast cancer cells are able to protect
themselves against vitamin D’s cancer-fighting chemistry by inhibiting
enzymes that activate it from 25OHD (calcidiol) into 1,25OHD (calcitriol) at
the cell margins. This effect was most pronounced when levels of 25OHD
outside the cell were low. The British researchers concluded that higher
levels of 25OHD outside the cell are needed in order to overcome the
cancer cell’s defense. When the cancer cell is faced with ample calcidiol,
the formation of more vitamin D receptors and activation of more calcitriol
tends to promote apoptosis and slow or even stop tumor growth.
If vitamin D is as important in fighting breast cancer as it appears to be,
and cancer cells have defenses against it, we should know if there are
environmental or dietary factors such as increased fluoride intake that
inhibit optimal D formation and activation, directly or indirectly.
Normal thyroid function is essential for normal D metabolism. Iodine and
selenium are required for normal thyroid function. According to the
National Research Council 2006 report, chronic hypothyroidism is reliably
induced with fluoride dosage from 0.01 mg/kg/day (exceeded with
consumption of fluoridated drinking water) when iodine or selenium is
deficient. Selenium deficiency can also cause hypothyroidism, and
selenium deficiency is known to increase risk of cancer incidence and
death. The body’s major detoxification pathways that protect against
cancer require selenium. Fluoride-induced thyroid suppression may be
one aspect of D deficiency despite supplementation, and may be related
to this fluoride-induced iodine and selenium deficiency.
Lastly, Vitamin D deficiency is one aspect of hypothyroidism and
autoimmune thyroid disease, which increase risk of both breast and
thyroid cancers. Supplementation with D can be therapeutic for both
hypothyroidism and autoimmune thyroid disease.
Reducing fluoride intake should therefore be considered as part of the
clinical strategy for prevention and treatment of breast cancer and thyroid
disease, and for optimization of vitamin D levels in the blood as well as
optimization of iodine and selenium intake.
References
Anticancer Res. 2006 Jul-Aug;26(4A):2573-80. Colston KW, Lowe LC, Mansi JL, Campbell MJ.
Vitamin D Status and Breast Cancer Risk
BACKGROUND: Local synthesis of 1alpha,25(OH)D3 in breast tissue may contribute to
maintenance of normal cell function and could be impaired with low circulating levels of the
precursor 25hydroxyvitamin D. The aims of this study were to: i) assess the association
between breast cancer risk and plasma 25OHD3 concentration and ii) define the significance of
expression of the 25OHD activating enzyme CYP27b1 in non-malignant and malignant models
of breast epithelial cells. MATERIALS AND METHODS: Breast cancer patients and control
women were recruited and their 25OHD levels measured by enzyme-linked immunosorbent
assay (ELISA). MRNA expression of CYP271b and the 1,25(OH)2D3 inactivating enzyme CYP24
were measured in breast cancer cell lines by RT-PCR and correlated with immunoblotting
approaches to the translated proteins. RESULTS: For women with 25OHD < 50 nM the odds
ratio for breast cancer compared with women with 25OHD > 50 nM was 3.54 (CI 1.89-6.61, p <
0.001). CYP271b and CYP24 were detected in non-malignant and malignant cell models.
Protein levels of 24OHase but not 1alphaOHase were decreased at confluence in the cell lines.
CONCLUSION: Impaired local generation of 1,25OHD3 may contribute to the development of
breast cancer.
Clinch CA. Fluoride Interactions with Iodine and Iodide: Implications for Breast Health. Fluoride
April-June 2009:42(2):75-87.
http://www.fluorideresearch.org/422/files/FJ2009_v42_n2_p00i-iii.pdf
Goodwin P. J. et al. Samuel Lunenfeld Research Institute, Toronto, ON, Canada; University of
Toronto, Toronto, ON, Canada; Sunnybrook Health Sciences Centre, Toronto, ON, Canada; St.
Michael's Hospital, Toronto, ON, Canada. Vitamin D deficiency is common at breast cancer
diagnosis and is associated with a significantly higher risk of distant recurrence and death in a
prospective cohort study of T1-3, N0-1, M0 BC.
Goodwin, P. (2009) Vitamin D in Cancer Patients: Above all, do no harm. Journal of Clinical
Oncology, Vol 27, No 13 (May 1), 2009: pp. 2117-2119
Graham, J.R., Burk, O., and Morin, P. (1987). A current restatement and continuing reappraisal
concerning demographic variables in American time-trend studies on water fluoridation and
human cancer. Proc Pennsylvania Academy of Sci. 61:138-146.
Johnson W, et al. (1979). Fluoridation and bone disease in renal patients. In: E Johansen, DR
Taves, TO Olsen, Eds. Continuing Evaluation of the Use of Fluorides. AAAS Selected
Symposium. Westview Press, Boulder, Colorado. pp. 275-293.
National Research Council. (2006). Fluoride in Drinking Water: A Scientific Review of EPA's
Standards. National Academies Press, Washington D.C.
Susheela, A.K. (2007) A Treatise on Fluorosis. Fluorosis Research and Rural Development
Foundation. Delhi, India.
Taylor A., Taylor N. (1965). Effects of Fluoride on Tumor Growth. Proceedings of Society of
Experimental Biol. and Medicine, Vol. 65 pp252-255.
Yiamouyiannis JA. (1993). Fluoridation and cancer: the biology and epidemiology of bone and
oral cancer related to fluoridation. Fluoride. 26(2):83-96. Full study at http://www.fluoridealert.
org/re/yiamouyiannis-1993.pdf
Yiamouyiannis J., Burk D. (1977) Fluoridation and cancer age-dependence of cancer mortality
related to artificial fluoridation, Fluoride 10: 102-124.
****
- These statements have not been evaluated by the U.S. Food & Drug Administration. The supplements
discussed are not intended to diagnose, treat, cure, or prevent any disease.
This website is intended as information only. The editors of this site are not medically-trained.
Please consult your licensed health care practitioner before implementing any health strategy.
The information provided on this site is designed to support, not replace, the relationship that
exists between a patient/site visitor and his/her existing physician. This site accepts no
advertising. Contents of this site copyrighted 2004-2015 by Breast Cancer Choices, Inc., a 501 (c) (3)
Nonprofit Organization.
Contact us with comments or for reprint permission at admin@breastcancerchoices.org
| announcements only. Your information will not be shared or sold to anyone. |
