segunda-feira, 1 de março de 2010
cancro mama, iodo,tiroide
01:20 | 
Publicada por
Luis Guerreiro
radiation therapy is palliative vs. curative
Posted on Feb 28th, 2010 by 
Bird
Birdhttp://health.groups.yahoo.com/group/breastcancerthinktank/message/3234
... Iodine is alkalizing to the system.
Barb F posted an article a few years ago describing how breast cancer, colon cancer and melanoma are in the same "family" of cancers. My mother had breast cancer and my sister had colon cancer. When people contact me from the internet, they often mention this cancer trifecta in their family.
Regarding radiation therapy, remember it has no survival value, may cause coronary artery problems and new cancers. Radiation is only used to reduce the rate of local recurrence in the breast over five years. People do not die from local recurrence. About 10 women out of a hundred will be spared local recurrence because of radiation. The 40% risk reduction number you may have been given is a misleading relative risk term. Read more about this here http://breastcancerchoices.org/faqtreatment.html
Radiation therapy is a short term, largely ineffective strategy with long term negative consequences with no survival advantage. If they come up with a kind of radiotherapy that isn't toxic, we will reconsider. Ductal lavage was in the works but I don't know what happened to it.
.... It goes without saying that cancer isn't a chemotherapy deficiency. It only puts out the fire, killing cells that are colonized or circulating. Chemo does absolutely nothing to address what caused cancer in the first place. And will continue to cause cancer.
The alternative community holds that something more radical than killing cells needs to be done-- by addressing the body's terrain and addressing what's wrong so patients don't get a recurrence.
One of the reasons I started pursuing iodine-deficiency as one of the underlying causes of some breast cancers is that iodine-sufficient animals would not get tumors. Breast-diseased animals given iodine would recover. As soon as iodine was withdrawn, the breasts got diseased again.
Iodine works in multiple, but very specific ways to nutritionally normalize receptors. It helps cancer cells die a normal "programmed death." It also keeps cancer cells from multiplying so fast. This has been shown in humans.
So after the emergency methods we sometimes use as temporary interventions- - we need to think about rebuilding a healthy host with the nutrients that are consistent with people who don't get cancer. We probably all won't agree about what strategies are most important but that doesn't matter. There is no absolute right strategy--which is why this group is called breastcancerthinktank and not "the place with all the answers."
... Iodine is alkalizing to the system.
Barb F posted an article a few years ago describing how breast cancer, colon cancer and melanoma are in the same "family" of cancers. My mother had breast cancer and my sister had colon cancer. When people contact me from the internet, they often mention this cancer trifecta in their family.
Regarding radiation therapy, remember it has no survival value, may cause coronary artery problems and new cancers. Radiation is only used to reduce the rate of local recurrence in the breast over five years. People do not die from local recurrence. About 10 women out of a hundred will be spared local recurrence because of radiation. The 40% risk reduction number you may have been given is a misleading relative risk term. Read more about this here http://breastcancerchoices.org/faqtreatment.html
Radiation therapy is a short term, largely ineffective strategy with long term negative consequences with no survival advantage. If they come up with a kind of radiotherapy that isn't toxic, we will reconsider. Ductal lavage was in the works but I don't know what happened to it.
.... It goes without saying that cancer isn't a chemotherapy deficiency. It only puts out the fire, killing cells that are colonized or circulating. Chemo does absolutely nothing to address what caused cancer in the first place. And will continue to cause cancer.
The alternative community holds that something more radical than killing cells needs to be done-- by addressing the body's terrain and addressing what's wrong so patients don't get a recurrence.
One of the reasons I started pursuing iodine-deficiency as one of the underlying causes of some breast cancers is that iodine-sufficient animals would not get tumors. Breast-diseased animals given iodine would recover. As soon as iodine was withdrawn, the breasts got diseased again.
Iodine works in multiple, but very specific ways to nutritionally normalize receptors. It helps cancer cells die a normal "programmed death." It also keeps cancer cells from multiplying so fast. This has been shown in humans.
So after the emergency methods we sometimes use as temporary interventions- - we need to think about rebuilding a healthy host with the nutrients that are consistent with people who don't get cancer. We probably all won't agree about what strategies are most important but that doesn't matter. There is no absolute right strategy--which is why this group is called breastcancerthinktank and not "the place with all the answers."
Access: PublicTagged with: breast cancer
This Is It
Posted on Feb 27th, 2010 by Bird
BirdI just saw the Michael Jackson video, "This is it."
As an artist that man is ethereal.
It's the way my macaw wraps his toes around his head when he's asking for some fondling. The look in a tiger's eye as he's sizing you up. The sunlight coming through the mist off the lake at dawn. I felt the spark.
As an artist that man is ethereal.
It's the way my macaw wraps his toes around his head when he's asking for some fondling. The look in a tiger's eye as he's sizing you up. The sunlight coming through the mist off the lake at dawn. I felt the spark.
is breast cancer an iodine deficiency disease?
Posted on Feb 27th, 2010 by Bird
Birdhttp://www.breastcancerchoices.org/iodine
Research suggests that some breast cancers may be an iodine deficiency disease.
As David Brownstein, MD, phrased it, "You cannot give breast cancer to rats that have sufficient iodine."
Research suggests that some breast cancers may be an iodine deficiency disease.
As David Brownstein, MD, phrased it, "You cannot give breast cancer to rats that have sufficient iodine."
Tagged with: breast cancer
estrogen inhibits iodine absorption
Posted on Feb 26th, 2010 by Bird
Birdhttp://www.youtube.com/watch?v=EoMfg76gAUo
Iodine Insufficiency and Cancer
Jorge D. Flechas MD
http://curezone.com/ig/i.asp?i=21726
Iodine Insufficiency and Cancer
Jorge D. Flechas MD
http://curezone.com/ig/i.asp?i=21726
Anemia in thyroid diseases
Posted on Feb 26th, 2010 by Bird
Birdhttp://www.ncbi.nlm.nih.gov/pubmed/1099360
Thyroid hormones generally stimulate erythropoiesis. These agents also increase erythrocyte 2,3-DPG concentrations, which serve to enhance the delivery of oxygen to tissues. In the absence of thyroid hormones, anemia frequently develops and may be normocytic, hypochromic-microcytic, or macrocytic. Anemia is an uncommon finding in hyperthyroidism but when present may be morphologically similar to that observed in hypothyroidism. Pernicious anemia has been strongly associated with hypothyroidism, hyperthyroidism, and thyroiditis. Complete correction of anemia often requires restoration of thyroid function as well as specific hematinic therapy. Continued attention to hematologic status is essential in the management of patients with thyroid diseases.
thyroid, iodine, and breast cancer
Posted on Feb 25th, 2010 by Bird
Birdhttp://web.ebscohost.com/ehost/detail?vid=3&hid=11&sid=5206e3a3-33aa-475b-a042-670998ce0551%40sessionmgr12&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#db=cmedm&AN=12927031
The thyroid, iodine and breast cancer.
A renewal of the search for a link between breast cancer and thyroid disease has once again demonstrated an increased prevalence of autoimmune thyroid disease in patients with breast cancer. This is the most recent of many studies showing an association between a variety of thyroid disorders and breast cancer. Such an association is not surprising as both diseases are female predominant with a similar postmenopausal peak incidence. The significance of the presence of thyroid autoantibodies, particularly thyroid peroxidase antibodies, in serum from patients with breast cancer is unknown, but it has been suggested that antibody positivity is associated with better prognosis. One area in which thyroid and breast functions overlap is in the uptake and utilization of dietary iodide. Experimental findings showing the ability of iodine or iodine-rich seaweed to inhibit breast tumour development is supported by the relatively low rate of breast cancer in Japanese women who consume a diet containing iodine-rich seaweed. However, there is as yet no direct evidence that iodine, iodinated compounds, or a combination of iodine and selenium is the antimammary carcinogenic element in the Japanese diet. It remains to be resolved whether the perceived breast cancer-thyroid disease relationship is thyroid or iodine related or, in the case of thyroid autoantibodies, is the consequence of an immune response to the carcinoma. Is this response breast specific and does it relate to iodine status? These and many other questions await resolution before a definitive role in the natural history of breast carcinoma can be assigned to the thyroid.
http://web.ebscohost.com/ehost/detail?vid=10&hid=4&sid=48257e09-d846-4ab1-8a05-a4940f309a3e%40sessionmgr4&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#db=cmedm&AN=16679319
Molecular iodine induces caspase-independent apoptosis in human breast carcinoma cells involving the mitochondria-mediated pathway.
Molecular iodine (I2) is known to inhibit the induction and promotion of N-methyl-n-nitrosourea-induced mammary carcinogenesis, to regress 7,12-dimethylbenz(a)anthracene-induced breast tumors in rat, and has also been shown to have beneficial effects in fibrocystic human breast disease. Cytotoxicity of iodine on cultured human breast cancer cell lines, namely MCF-7, MDA-MB-231, MDA-MB-453, ZR-75-1, and T-47D, is reported in this communication. Iodineapoptosis in all of the cell lines tested, except MDA-MB-231, shown by sub-G1 peak analysis using flow cytometry. Iodine inhibited proliferation of normal humancells; however, it did not induce apoptosis incells. The iodine-induced apoptotic mechanism was studied in MCF-7 cells. DNA fragmentation analysis confirmed internucleosomal DNA degradation. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling established that iodine induced apoptosis in a time- and dose-dependent manner in MCF-7 cells. Iodine-induced apoptosis was independent of caspases. Iodinein total cellular thiol content. Western blot results showed a decrease in Bcl-2 and up-regulation of Bax. Immunofluorescence studies confirmed the activation and mitochondrial membrane localization of Bax. Ectopic Bcl-2 overexpression did not rescue iodine-induced cell death. Iodine treatment inducesthe translocation of apoptosis-inducing factor from mitochondria to the nucleus, and treatment of N-acetyl-L-cysteine prior to iodineapoptosis-inducing factor and subsequently cell death, indicating that thiol depletion may play an important role in iodine-induced cell death. These results demonstrate that iodine treatment activates a caspase-independent and mitochondria-mediatedpathway.
http://web.ebscohost.com/ehost/detail?vid=5&hid=4&sid=bd9cc47a-cdbc-4876-93c7-235300aa1398%40sessionmgr10&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#db=cmedm&AN=16025225
Is iodine a gatekeeper of the integrity of the mammary gland?
This paper reviews evidence showing induced these dissipated mitochondrial membrane potential, exhibited antioxidant activity, and caused depletion apoptotic iodine as an antioxidant and antiproliferative agent contributing to the integrity of normal mammary gland. Seaweed is an important dietary component in Asian communities and a rich source of iodine in several chemical forms. The high consumption of this element (25 times more than in Occident) has been associated with the low incidence of benign and cancer breast disease in Japanese women. In animal and human studies, molecular iodine (I(2)) supplementation exerts a suppressive effect on the development and size of both benign and cancerIodine, in addition to its incorporation into thyroid hormones, is bound into antiproliferative iodolipids in the thyroid called iodolactones, which may also play a role in the proliferative control of mammary gland. We propose that an I(2) supplement should be considered as an adjuvant in breast cancer therapy.
http://web.ebscohost.com/ehost/detail?vid=9&hid=4&sid=bd9cc47a-cdbc-4876-93c7-235300aa1398%40sessionmgr10&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#db=cmedm&AN=14757962
Role of iodine in antioxidant defence in thyroid and breast disease
The role played in thyroid hormonogenesis by iodide oxidation to iodineIodine deficiency may produce conditions of oxidative stress with high TSH producing a level of H_2O_2, which because of lack of iodide is not being used to form thyroid hormones. The cytotoxic actions of excess iodide in thyroid cells may depend on the formation of free radicals and can be attributed to both necrotic and apoptotic mechanisms with necrosis predominating in goiter development and apoptosis during iodide induced involution. These cytotoxic effects appear to depend on the status of antioxidative enzymes and may only be evident in conditions of selenium deficiency where the activity of selenium containing antioxidative enzymes is impaired. Less compelling evidence exists of a role for iodide as an antioxidant in the breast. However the Japanese experience may indicate a protective effect against breast cancer for an iodine rich seaweed containing diet. Similarly thyroid autoimmunity may also be associated with improved prognosis. Whether this phenomenon is breast specific and its possible relationship to iodine or selenium status awaits resolution.
http://web.ebscohost.com/ehost/detail?vid=11&hid=4&sid=48257e09-d846-4ab1-8a05-a4940f309a3e%40sessionmgr4&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#db=cmedm&AN=17243118
Enhanced tight junction function in human breast cancer cells by antioxidant, selenium and polyunsaturated lipid.
Paracellular permeability (PCP) is governed by tight junctions (TJs) in epithelial cells, acting as cell-cell adhesion structures, the aberration of which is known to be linked to the dissociation and metastasis of breast cancer cells. This study hypothesized that the function of TJs in human breast cancer cells can be augmented by gamma linolenic acid (GLA), selenium (Se), and iodine (I) in the presence of 17-beta-estradiol, as these molecules are known to increase TJ functions in endothelial cells, using assays of trans-epithelial resistance (TER), PCP, immunofluorescence, and in vitro invasion and motility models. GLA, I, and Se individually increased TER of MDA-MB-231 and MCF-7 human breast cancer cells. The combination of all three agents also had a significant increase in TER. Addition of GLA/Se/I reduced PCP of both breast cancer cell lines. GLA/Se/I reversed the effect of 17-beta-estradiol (reduced TER, increased PCP). Immunofluorescence revealed that after treatment with Se/I/GLA over 24 h, there was increasing relocation to breast cancer cell-cell junctions of occludin and ZO-1 in MCF-7 cells. Moreover, treatment with GLA/Se/I, alone or in combination, significantly reduced in vitro invasion of MDA-MB-231 cells through an endothelial cell barrier (P < 0.0001) and reduced 17-beta-estradiol induced breast cancer cell motility (P < 0.0001). Our previous work has demonstrated that GLA, I, and Se alone, or in combination are able to strengthen the function of TJs in human endothelial cells; this has now proved to be true of human breast cancer cells. This combination also completely reversed the effect of 17-beta-estradiol in these cells. ((c) 2007 Wiley-Liss, Inc.)
http://web.ebscohost.com/ehost/detail?vid=11&hid=4&sid=48257e09-d846-4ab1-8a05-a4940f309a3e%40sessionmgr4&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#db=cmedm&AN=3067061
Di-iodothyronine as part of the oestradiol and catechol oestrogen receptor--the role of iodine, thyroid hormones and melatonin in the aetiology of breast cancer.
Hypothyroidism and low iodine intake may be important aetiological factors in oestrogen dependent tumours of the breast, uterus and ovary. They are preventable risk factors. Iodine supplementation will hopefully lead to a decreased incidence of these cancers in future generations. The present author proposes that the tyrosyl residue in the hydrophobic oestrogen binding site of the oestrogen receptor is post translationally modified to monoiodotyrosine and hence 3,3' di-iodothyronine monoamine (T2) by peroxidase activity. He has previously proposed that various monoamine receptors are also T2 based. The densities of these receptors are increased in hypothyroidism and they exert control over release of prolactin and other hormones, including melatonin at multiple sites in the hypothalamic--pituitary axis. Melatonin is a metabolite of serotonin and hence melatonin receptors may be T2 or rT3 based as well. These factors could be significant in the aetiology of breastcancer as high prolactin and melatonin levels may be protective. Oestrogen receptor density may be increased in hypothyroidism as is certain monoamine receptor density. This would amplify the effect of high circulation oestrogen levels in hypothyroidism and may help explain why hypothyroidism and low iodine intake are risk factors for breast, uterine and ovarian cancer.
peripheral blood mononuclear exposure restored basal thiol content, ROS levels, and completely inhibited nuclear translocation of neoplasias. This effect is accompanied by a significant reduction in cellular lipoperoxidation. (organification) is well established.
http://web.ebscohost.com/ehost/detail?vid=13&hid=4&sid=48257e09-d846-4ab1-8a05-a4940f309a3e%40sessionmgr4&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#db=cmedm&AN=18645607
Iodine alters gene expression in the MCF7 breast cancer cell line: evidence for an anti-estrogen effect of iodine.
The protective effects of iodine on breast cancer have been postulated from epidemiologic evidence and described in animal models. The molecular mechanisms responsible have not been identified but laboratory evidence suggests that iodine may inhibit cancer promotion through modulation of the estrogen pathway. To elucidate the role of iodine in breast cancer, the effect of Lugol's iodinebreast cancer cell line. Microarray analysis identified 29 genes that were up-regulated and 14 genes that were down-regulated in response to iodine/iodide treatment. The altered genes included several involved in hormone metabolism as well as genes involved in the regulation of cell cycle progression, growth and differentiation. Quantitative RT-PCR confirmed the array data demonstrating that iodine/iodide treatment increased the mRNA levels of several genes involved in estrogen metabolism (CYP1A1, CYP1B1, and AKR1C1) while decreasing the levels of the estrogen responsive genes TFF1 and WISP2. This report presents the results of the first gene array profiling of the response of a breast cancer cell line to iodine treatment. In addition to elucidating our understanding of the effects of iodine/iodide on breast cancer, this work suggests that iodine/iodide may be useful as an adjuvant therapy in the pharmacologic manipulation of the estrogen pathway in women with breast cancer.
http://web.ebscohost.com/ehost/detail?vid=13&hid=4&sid=48257e09-d846-4ab1-8a05-a4940f309a3e%40sessionmgr4&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#db=cmedm&AN=18676157
Role of lipid peroxidation and oxidative stress in the association between thyroid diseases and breast cancer.
Evidence is accumulating for a role of the thyroid in the natural history of breastcancer, although no plausible mechanism has been advanced to explain this association. We believe that the thyroid disease-breast cancer relationship provides a unique opportunity to find out the causes of breast cancer. Both diseases are female predominant, with specifically identified biological pathways and genetic and environmental determinants, and seeing them in concert provides an opportunity to identify the most relevant mechanistic pathways. In this communication, we advance a plausible mechanism to explain the thyroid disease-breast cancer relationship. We specifically propose that the reduction in risk associated with hyperthyroidism or increased levels of thyroid hormones, or iodine, may derive from the pro-oxidant properties of these compounds, i.e., from its ability to generate oxidative stress-induced apoptosis. Conversely, the increased risk from hypothyroidism may derive from its ability to inhibit this stress-mediated apoptotic process.
http://web.ebscohost.com/ehost/detail?vid=16&hid=105&sid=48257e09-d846-4ab1-8a05-a4940f309a3e%40sessionmgr4&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#db=cmedm&AN=17956159
Uptake and gene expression with antitumoral doses of iodine in thyroid and mammary gland: evidence that chronic administration has no harmful effects.
Several studies have demonstrated that moderately high concentrations of molecular iodine (I(2)) diminish the symptoms of mammary fibrosis in women, reduce the occurrence of mammary cancer induced chemically in rats (50-70%), and have a clear antiproliferative and apoptotic effect in the human tumoral mammary cell line MCF-7. Nevertheless, the importance of these effects has been underestimated, in part because of the notion that exposure to excess iodineiodine differ in an organ-specific manner and also depend on the chemical form of the iodine ingested (potassium iodide vs. I(2)). Further, we show that a moderately high I(2) supplement (0.05%) causes some of the characteristics of the "acute Wolff-Chaikoff effect"; namely, it lowers expression of the sodium/iodide symporter, pendrin, thyroperoxidase (TPO), and deiodinase type 1 in thyroid gland without diminishing circulating levels of thyroid hormone. Finally, we confirm that I(2) metabolism is independent of TPO, and we demonstrate that, at the doses used here, which are potentially useful to treat mammary tumors, chronic I(2) supplement is not accompanied by any harmful secondary effects on the thyroid or general physiology. Thus, we suggest that I(2) could be considered for use in clinical trials of breast cancer therapies. solution (5% I(2), 10% KI) on gene expression was analyzed in the estrogen responsive MCF-7 represents a potential risk to thyroid physiology. In the present work we demonstrate that uptake and metabolism of
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC314438/
http://health.groups.yahoo.com/group/iodine/
The thyroid, iodine and breast cancer.
A renewal of the search for a link between breast cancer and thyroid disease has once again demonstrated an increased prevalence of autoimmune thyroid disease in patients with breast cancer. This is the most recent of many studies showing an association between a variety of thyroid disorders and breast cancer. Such an association is not surprising as both diseases are female predominant with a similar postmenopausal peak incidence. The significance of the presence of thyroid autoantibodies, particularly thyroid peroxidase antibodies, in serum from patients with breast cancer is unknown, but it has been suggested that antibody positivity is associated with better prognosis. One area in which thyroid and breast functions overlap is in the uptake and utilization of dietary iodide. Experimental findings showing the ability of iodine or iodine-rich seaweed to inhibit breast tumour development is supported by the relatively low rate of breast cancer in Japanese women who consume a diet containing iodine-rich seaweed. However, there is as yet no direct evidence that iodine, iodinated compounds, or a combination of iodine and selenium is the antimammary carcinogenic element in the Japanese diet. It remains to be resolved whether the perceived breast cancer-thyroid disease relationship is thyroid or iodine related or, in the case of thyroid autoantibodies, is the consequence of an immune response to the carcinoma. Is this response breast specific and does it relate to iodine status? These and many other questions await resolution before a definitive role in the natural history of breast carcinoma can be assigned to the thyroid.
http://web.ebscohost.com/ehost/detail?vid=10&hid=4&sid=48257e09-d846-4ab1-8a05-a4940f309a3e%40sessionmgr4&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#db=cmedm&AN=16679319
Molecular iodine induces caspase-independent apoptosis in human breast carcinoma cells involving the mitochondria-mediated pathway.
Molecular iodine (I2) is known to inhibit the induction and promotion of N-methyl-n-nitrosourea-induced mammary carcinogenesis, to regress 7,12-dimethylbenz(a)anthracene-induced breast tumors in rat, and has also been shown to have beneficial effects in fibrocystic human breast disease. Cytotoxicity of iodine on cultured human breast cancer cell lines, namely MCF-7, MDA-MB-231, MDA-MB-453, ZR-75-1, and T-47D, is reported in this communication. Iodineapoptosis in all of the cell lines tested, except MDA-MB-231, shown by sub-G1 peak analysis using flow cytometry. Iodine inhibited proliferation of normal humancells; however, it did not induce apoptosis incells. The iodine-induced apoptotic mechanism was studied in MCF-7 cells. DNA fragmentation analysis confirmed internucleosomal DNA degradation. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling established that iodine induced apoptosis in a time- and dose-dependent manner in MCF-7 cells. Iodine-induced apoptosis was independent of caspases. Iodinein total cellular thiol content. Western blot results showed a decrease in Bcl-2 and up-regulation of Bax. Immunofluorescence studies confirmed the activation and mitochondrial membrane localization of Bax. Ectopic Bcl-2 overexpression did not rescue iodine-induced cell death. Iodine treatment inducesthe translocation of apoptosis-inducing factor from mitochondria to the nucleus, and treatment of N-acetyl-L-cysteine prior to iodineapoptosis-inducing factor and subsequently cell death, indicating that thiol depletion may play an important role in iodine-induced cell death. These results demonstrate that iodine treatment activates a caspase-independent and mitochondria-mediatedpathway.
http://web.ebscohost.com/ehost/detail?vid=5&hid=4&sid=bd9cc47a-cdbc-4876-93c7-235300aa1398%40sessionmgr10&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#db=cmedm&AN=16025225
Is iodine a gatekeeper of the integrity of the mammary gland?
This paper reviews evidence showing induced these dissipated mitochondrial membrane potential, exhibited antioxidant activity, and caused depletion apoptotic iodine as an antioxidant and antiproliferative agent contributing to the integrity of normal mammary gland. Seaweed is an important dietary component in Asian communities and a rich source of iodine in several chemical forms. The high consumption of this element (25 times more than in Occident) has been associated with the low incidence of benign and cancer breast disease in Japanese women. In animal and human studies, molecular iodine (I(2)) supplementation exerts a suppressive effect on the development and size of both benign and cancerIodine, in addition to its incorporation into thyroid hormones, is bound into antiproliferative iodolipids in the thyroid called iodolactones, which may also play a role in the proliferative control of mammary gland. We propose that an I(2) supplement should be considered as an adjuvant in breast cancer therapy.
http://web.ebscohost.com/ehost/detail?vid=9&hid=4&sid=bd9cc47a-cdbc-4876-93c7-235300aa1398%40sessionmgr10&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#db=cmedm&AN=14757962
Role of iodine in antioxidant defence in thyroid and breast disease
The role played in thyroid hormonogenesis by iodide oxidation to iodineIodine deficiency may produce conditions of oxidative stress with high TSH producing a level of H_2O_2, which because of lack of iodide is not being used to form thyroid hormones. The cytotoxic actions of excess iodide in thyroid cells may depend on the formation of free radicals and can be attributed to both necrotic and apoptotic mechanisms with necrosis predominating in goiter development and apoptosis during iodide induced involution. These cytotoxic effects appear to depend on the status of antioxidative enzymes and may only be evident in conditions of selenium deficiency where the activity of selenium containing antioxidative enzymes is impaired. Less compelling evidence exists of a role for iodide as an antioxidant in the breast. However the Japanese experience may indicate a protective effect against breast cancer for an iodine rich seaweed containing diet. Similarly thyroid autoimmunity may also be associated with improved prognosis. Whether this phenomenon is breast specific and its possible relationship to iodine or selenium status awaits resolution.
http://web.ebscohost.com/ehost/detail?vid=11&hid=4&sid=48257e09-d846-4ab1-8a05-a4940f309a3e%40sessionmgr4&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#db=cmedm&AN=17243118
Enhanced tight junction function in human breast cancer cells by antioxidant, selenium and polyunsaturated lipid.
Paracellular permeability (PCP) is governed by tight junctions (TJs) in epithelial cells, acting as cell-cell adhesion structures, the aberration of which is known to be linked to the dissociation and metastasis of breast cancer cells. This study hypothesized that the function of TJs in human breast cancer cells can be augmented by gamma linolenic acid (GLA), selenium (Se), and iodine (I) in the presence of 17-beta-estradiol, as these molecules are known to increase TJ functions in endothelial cells, using assays of trans-epithelial resistance (TER), PCP, immunofluorescence, and in vitro invasion and motility models. GLA, I, and Se individually increased TER of MDA-MB-231 and MCF-7 human breast cancer cells. The combination of all three agents also had a significant increase in TER. Addition of GLA/Se/I reduced PCP of both breast cancer cell lines. GLA/Se/I reversed the effect of 17-beta-estradiol (reduced TER, increased PCP). Immunofluorescence revealed that after treatment with Se/I/GLA over 24 h, there was increasing relocation to breast cancer cell-cell junctions of occludin and ZO-1 in MCF-7 cells. Moreover, treatment with GLA/Se/I, alone or in combination, significantly reduced in vitro invasion of MDA-MB-231 cells through an endothelial cell barrier (P < 0.0001) and reduced 17-beta-estradiol induced breast cancer cell motility (P < 0.0001). Our previous work has demonstrated that GLA, I, and Se alone, or in combination are able to strengthen the function of TJs in human endothelial cells; this has now proved to be true of human breast cancer cells. This combination also completely reversed the effect of 17-beta-estradiol in these cells. ((c) 2007 Wiley-Liss, Inc.)
http://web.ebscohost.com/ehost/detail?vid=11&hid=4&sid=48257e09-d846-4ab1-8a05-a4940f309a3e%40sessionmgr4&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#db=cmedm&AN=3067061
Di-iodothyronine as part of the oestradiol and catechol oestrogen receptor--the role of iodine, thyroid hormones and melatonin in the aetiology of breast cancer.
Hypothyroidism and low iodine intake may be important aetiological factors in oestrogen dependent tumours of the breast, uterus and ovary. They are preventable risk factors. Iodine supplementation will hopefully lead to a decreased incidence of these cancers in future generations. The present author proposes that the tyrosyl residue in the hydrophobic oestrogen binding site of the oestrogen receptor is post translationally modified to monoiodotyrosine and hence 3,3' di-iodothyronine monoamine (T2) by peroxidase activity. He has previously proposed that various monoamine receptors are also T2 based. The densities of these receptors are increased in hypothyroidism and they exert control over release of prolactin and other hormones, including melatonin at multiple sites in the hypothalamic--pituitary axis. Melatonin is a metabolite of serotonin and hence melatonin receptors may be T2 or rT3 based as well. These factors could be significant in the aetiology of breastcancer as high prolactin and melatonin levels may be protective. Oestrogen receptor density may be increased in hypothyroidism as is certain monoamine receptor density. This would amplify the effect of high circulation oestrogen levels in hypothyroidism and may help explain why hypothyroidism and low iodine intake are risk factors for breast, uterine and ovarian cancer.
peripheral blood mononuclear exposure restored basal thiol content, ROS levels, and completely inhibited nuclear translocation of neoplasias. This effect is accompanied by a significant reduction in cellular lipoperoxidation. (organification) is well established.
http://web.ebscohost.com/ehost/detail?vid=13&hid=4&sid=48257e09-d846-4ab1-8a05-a4940f309a3e%40sessionmgr4&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#db=cmedm&AN=18645607
Iodine alters gene expression in the MCF7 breast cancer cell line: evidence for an anti-estrogen effect of iodine.
The protective effects of iodine on breast cancer have been postulated from epidemiologic evidence and described in animal models. The molecular mechanisms responsible have not been identified but laboratory evidence suggests that iodine may inhibit cancer promotion through modulation of the estrogen pathway. To elucidate the role of iodine in breast cancer, the effect of Lugol's iodinebreast cancer cell line. Microarray analysis identified 29 genes that were up-regulated and 14 genes that were down-regulated in response to iodine/iodide treatment. The altered genes included several involved in hormone metabolism as well as genes involved in the regulation of cell cycle progression, growth and differentiation. Quantitative RT-PCR confirmed the array data demonstrating that iodine/iodide treatment increased the mRNA levels of several genes involved in estrogen metabolism (CYP1A1, CYP1B1, and AKR1C1) while decreasing the levels of the estrogen responsive genes TFF1 and WISP2. This report presents the results of the first gene array profiling of the response of a breast cancer cell line to iodine treatment. In addition to elucidating our understanding of the effects of iodine/iodide on breast cancer, this work suggests that iodine/iodide may be useful as an adjuvant therapy in the pharmacologic manipulation of the estrogen pathway in women with breast cancer.
http://web.ebscohost.com/ehost/detail?vid=13&hid=4&sid=48257e09-d846-4ab1-8a05-a4940f309a3e%40sessionmgr4&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#db=cmedm&AN=18676157
Role of lipid peroxidation and oxidative stress in the association between thyroid diseases and breast cancer.
Evidence is accumulating for a role of the thyroid in the natural history of breastcancer, although no plausible mechanism has been advanced to explain this association. We believe that the thyroid disease-breast cancer relationship provides a unique opportunity to find out the causes of breast cancer. Both diseases are female predominant, with specifically identified biological pathways and genetic and environmental determinants, and seeing them in concert provides an opportunity to identify the most relevant mechanistic pathways. In this communication, we advance a plausible mechanism to explain the thyroid disease-breast cancer relationship. We specifically propose that the reduction in risk associated with hyperthyroidism or increased levels of thyroid hormones, or iodine, may derive from the pro-oxidant properties of these compounds, i.e., from its ability to generate oxidative stress-induced apoptosis. Conversely, the increased risk from hypothyroidism may derive from its ability to inhibit this stress-mediated apoptotic process.
http://web.ebscohost.com/ehost/detail?vid=16&hid=105&sid=48257e09-d846-4ab1-8a05-a4940f309a3e%40sessionmgr4&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#db=cmedm&AN=17956159
Uptake and gene expression with antitumoral doses of iodine in thyroid and mammary gland: evidence that chronic administration has no harmful effects.
Several studies have demonstrated that moderately high concentrations of molecular iodine (I(2)) diminish the symptoms of mammary fibrosis in women, reduce the occurrence of mammary cancer induced chemically in rats (50-70%), and have a clear antiproliferative and apoptotic effect in the human tumoral mammary cell line MCF-7. Nevertheless, the importance of these effects has been underestimated, in part because of the notion that exposure to excess iodineiodine differ in an organ-specific manner and also depend on the chemical form of the iodine ingested (potassium iodide vs. I(2)). Further, we show that a moderately high I(2) supplement (0.05%) causes some of the characteristics of the "acute Wolff-Chaikoff effect"; namely, it lowers expression of the sodium/iodide symporter, pendrin, thyroperoxidase (TPO), and deiodinase type 1 in thyroid gland without diminishing circulating levels of thyroid hormone. Finally, we confirm that I(2) metabolism is independent of TPO, and we demonstrate that, at the doses used here, which are potentially useful to treat mammary tumors, chronic I(2) supplement is not accompanied by any harmful secondary effects on the thyroid or general physiology. Thus, we suggest that I(2) could be considered for use in clinical trials of breast cancer therapies. solution (5% I(2), 10% KI) on gene expression was analyzed in the estrogen responsive MCF-7 represents a potential risk to thyroid physiology. In the present work we demonstrate that uptake and metabolism of
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC314438/
A renewal of the search for a link between breast cancer and thyroid disease has once again demonstrated an increased prevalence of autoimmune thyroid disease in patients with breast cancer. This is the most recent of many studies showing an association between a variety of thyroid disorders and breast cancer. Such an association is not surprising as both diseases are female predominant with a similar postmenopausal peak incidence. The significance of the presence of thyroid autoantibodies, particularly thyroid peroxidase antibodies, in serum from patients with breast cancer is unknown, but it has been suggested that antibody positivity is associated with better prognosis. One area in which thyroid and breast functions overlap is in the uptake and utilization of dietary iodide. Experimental findings showing the ability of iodine or iodine-rich seaweed to inhibit breast tumour development is supported by the relatively low rate of breast cancer in Japanese women who consume a diet containing iodine-rich seaweed. However, there is as yet no direct evidence that iodine, iodinated compounds, or a combination of iodine and selenium is the antimammary carcinogenic element in the Japanese diet. It remains to be resolved whether the perceived breast cancer–thyroid disease relationship is thyroid or iodine related or, in the case of thyroid autoantibodies, is the consequence of an immune response to the carcinoma. Is this response breast specific and does it relate to iodine status? These and many other questions await resolution before a definitive role in the natural history of breast carcinoma can be assigned to the thyroid.
Abstract
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.
http://health.groups.yahoo.com/group/iodine/
Iodine and human nutrition. How much iodine do we need? What are the best sources? What happens if we don't get enough iodine? Or get too much?
http://community.breastcancer.org/forum/79/topic/729108?page=5
Dx 1/19/2009, IDC, 2cm, Stage IIIa, Grade 2, 6/10 nodes, ER+/PR+, HER2-
Iodine has been found effective with hypothyroid and hyperthyroid conditions, goiter, fibrocystic breasts, uterine fibroids, ovarian cysts, brain fog, constipation, obesity, diabetes, cancer, high blood pressure, arrhythmias like atrial fibrillation, and detoxification issues (mercury, perchlorate, fluoride, bromide).
Iodine is detected in every organ and tissue in the body and is essential in pregnancy. It is found in high levels in the thyroid gland, breast, ovaries, liver, lung, heart, stomach, and adrenal glands.
There is currently a great deal of research on iodine and cancer, including cancer of the breast, colon, lungs, ovaries, pancreas, prostate, stomach, and thyroid.
Some doctors are now using iodine in the treatment of children with down syndrome as well as autism with positive results.
The Iodine Group has hundreds of links to relevant information and research. You can also find iodine information on our sister website: www.iodine4health.com
If you an an Iodine Researcher, you may be interested in our subgroup, IodineResearch: http://tech.groups.yahoo.com/group/IodineResearch/
About the owner: I am a 9 yr thyroid cancer survivor saved by iodine. Treated with 3 rounds of RAI and still had registering Tg markers. In 2006 when my markers rose my endo recommended external beam radition. I needed something different. I sought the help of Dr. David Brownstein - one of the pioneers in iodine. He placed me on 50 mgs of iodine, balanced my hormones, switched me from Synthroid to Armour and started a nutritional balancing program. I removed 11 amalgams and a root canal tooth. Today I am feeling better than I have in years! Join us!
To your health!
Stephanie
www.naturalthyroidchoices.com
and
When humans lack iodine the thyroid gland enlarges (goiter), nodules appear in the thyroid gland and over a period of time cancer may appear in a thyroid nodule. Conventional medicine treats thyroid gland enlargement with thyroid hormone without considering the possibility that the hypothyroidism and goiter may be due to lack of iodine. This failure to diagnose and treat iodine deficiency can lead to an increased risk of breast cancer and the longer the diagnosis is missed the greater the chance that breast cancer will occur.
Iodine has a role in promoting general well being as well as protecting against infections, degenerative diseases and cancer. Iodine promotes the normal killing of defective and abnormal cells (apoptosis). Thus, iodine helps the body's surveillance system to detect and remove abnormal cells. Additionally, the presence of iodine triggers differentiation away from the more dangerous undifferentiated type of cell toward normal cells. The presence of adequate levels of iodine in the body (Japanese diet with lots of sea vegetables and fish) reduces reactive oxygen species (ROS). in the body which decreases the oxidative burden in the body This results in slowing of degeneration disease processes and decreasing the risk of cancer.
By Dr. James Howenstine, MD.
July 27, 2006
NewsWithViews.com
July 27, 2006
NewsWithViews.com
on the same thread ....
Both thyroid cancer and breast cancer are iodine deficiency diseases.
Women who have had thyroid cancer have a significant increase in the risk of breast cancer, especially for women ages 30 to 34, according to a report in the journal Cancer(Vol. 92, No. 2: 225-31).
Amy Chen, MD, and her colleagues from the departments of head and neck surgery, biomathematics, epidemiology, and endocrinology at the M. D. Anderson Cancer Center in Houston, wanted to find out whether or not there was a higher incidence of breast cancer in women who were previously treated for thyroid cancer, or if women who had breast cancer had a higher incidence of subsequent thyroid cancer. Both cancers are most frequently found in women, but only a single study had suggested there might be some relationship between the two.
The researchers examined information from the National Cancer Institute's SEER (Surveillance, Epidemiology, and End Results) database (which collects cancer information from 14 different regions of the country and covers about 14% of the US population). They examined the records of 365 women with both thyroid and breast cancer diagnosed between January 1973 and December 1994.
Breast Cancer Followed the Thyroid CancerThe authors report that when the first cancer diagnosed was breast cancer, there was no subsequent increase in thyroid cancer. However, when the situation was reversed, and thyroid cancer was the first cancer diagnosed and breast cancer the second, there was a significant increase in the risk of breast cancer, in particular in women aged 30 to 34 where the risk was 1.9 times that expected for women in the same age group who had not had thyroid cancer.
The researchers also noted that this increased risk was found only in white, premenopausal women. Similar increases were not noted in African-American women (although the numbers of cases in this group was small). The greatest increased risk of breast cancer was found 15 to 20 years after the diagnosis and treatment of the thyroid cancer.
More Research Is NeededWhy this relationship exists is uncertain, according to the authors, who note their concern regarding the potential role of radioactive iodine in the treatment of the thyroid cancer as a possible factor.
Another possibility, the authors suggest, is that similar exposures to something in the environment may cause the relationship, but this is less likely since women diagnosed first with breast cancer did not later develop increased numbers of thyroid cancers.
What is important, the authors conclude at this time, is that these women and their physicians remember the importance of lifetime monitoring and cancer screening.
Source: American Cancer Society
http://www.cancer.org/docroot/NWS/content/NWS_1_1x_Thyroid_Cancer_and_Breast_Cancer_Linked_in_Women.asp
and on the same thread ....
The iodine and thyroid hormone
defencehttp://www.femail.com.au/breast_cancer_iodine_thyroid_connection.htm
As long as a woman's thyroid gland is working well, the cancer in situ stays in the breast and does not cause any problems. If the cancer goes to the second phase, it spreads through the surrounding connective tissue,3 so the strength and function of this connective tissue barrier are important. Connective tissue is controlled by thyroid hormone. If the connective tissue level of thyroid hormone is high, then the defence of connective tissue is strong, and the cancer cannot spread. Thus the spread of cancer can be inhibited by giving exogenous thyroid hormone.
Most of the potential environmental causes of breast cancer, such as pesticides and estrogen-like compounds in the environment, have been found to be only a small factor in causing breast cancer. However, if a person has enough iodine flowing through the body systems, the toxins cannot do much damage because iodine is one of the greatest inactivators of chemical toxins.
In the second phase of the cancer process, distant metastases,5 such as the spread of cancer to the lungs or brain, almost invariably involve connective tissue.3 When working properly, the connective tissue serves as a barrier to cancer cell migration. Since the edema6 of severe hypothyroid states is located in the connective tissue of all organs, it has been assumed and then proven in more recent years that thyroid hormone is the main controller of connective tissue function.
At levels of two to three milligrams of dietary iodine per day, the thyroid gland becomes saturated, and most of the iodine then bathes the extracellular compartment, triggering apoptosis4 by means of an old (in terms of evolution) reaction between iodine and tyrosine, or iodine and histidine-the same chemical reaction by which iodine in dilute solutions causes the death of bacteria and all other single-celled organisms, such as bacteria of all types, viruses, fungi, and protozoa.
As long as a woman's thyroid gland is working well, the cancer in situ stays in the breast and does not cause any problems. If the cancer goes to the second phase, it spreads through the surrounding connective tissue,3 so the strength and function of this connective tissue barrier are important. Connective tissue is controlled by thyroid hormone. If the connective tissue level of thyroid hormone is high, then the defence of connective tissue is strong, and the cancer cannot spread. Thus the spread of cancer can be inhibited by giving exogenous thyroid hormone.
Most of the potential environmental causes of breast cancer, such as pesticides and estrogen-like compounds in the environment, have been found to be only a small factor in causing breast cancer. However, if a person has enough iodine flowing through the body systems, the toxins cannot do much damage because iodine is one of the greatest inactivators of chemical toxins.
In the second phase of the cancer process, distant metastases,5 such as the spread of cancer to the lungs or brain, almost invariably involve connective tissue.3 When working properly, the connective tissue serves as a barrier to cancer cell migration. Since the edema6 of severe hypothyroid states is located in the connective tissue of all organs, it has been assumed and then proven in more recent years that thyroid hormone is the main controller of connective tissue function.
At levels of two to three milligrams of dietary iodine per day, the thyroid gland becomes saturated, and most of the iodine then bathes the extracellular compartment, triggering apoptosis4 by means of an old (in terms of evolution) reaction between iodine and tyrosine, or iodine and histidine-the same chemical reaction by which iodine in dilute solutions causes the death of bacteria and all other single-celled organisms, such as bacteria of all types, viruses, fungi, and protozoa.
and from the same thread ...
Most thyroid disease goes undiagnosed if the doctor only relies on blood tests. As I wrote above, a good practitioner diagnoses from the list of symptoms associated with thyroid disease.
Breast diseases are not caused by thyroid disease. BOTH DISEASES ARE A RESULT OF THE SAME DEFICIENCY. You can Google breast iodine and read up.
Iodine has been given for fibrocystic breast disease since the 90s. Because of the Mayo Clinic research, we now know some forms of fibrocystic disease progress to breast cancer. So the goal is to stop any new cancers by arresting sick breasts before so-called benign conditions progress.
Also: A recent study showed iodine reduced cancer cell proliferation in patients during the period between biopsy and surgery.
There is a lot of info here: www.breastcancerchoices.org/iodine
and from the same thread ....http://community.breastcancer.org/forum/79/topic/729108?page=5
I just got off the phone with Dr Flechas a couple of hours ago. Based on my iodine levels, he suggested that I do 50mg of Iodoral twice a day, along with ATP Cofactor. He said that the ATP Cofactor is B vitamins that help the 2 forms of iodine in Iodoral stick to and break down the protein around cancer. He told me that the best follow-up would be retesting the 24-hour urine test in 2-3 months, to see what my saturation point was then. He said adjustments might be needed, but most BC patients should plan on doing Iodoral for life, as it is about 80% effective in preventing recurrances. I forgot to ask if he meant in BC or in all cancer. (Chemo brain). He is willing to work with your doctor, or you can continue to use him for phone consultations.
So if you are curious, or want to know for yourself, the test costs $42, which breastcancerchoices.org will reimburse you for if you have BC, and are willing to let them use your information for research. Breastcancerchoices.org has the cheapest price of Iodoral, and uses any profits to help fund further research on the links between iodine and breast cancer.
Dx 1/19/2009, IDC, 2cm, Stage IIIa, Grade 2, 6/10 nodes, ER+/PR+, HER2-
and on the same thread ....
From the San Antonio Breast Cancer symposium
Iodine given to breast cancer patients for two to five weeks before surgery decreased cell proliferation and increased cell death (good) in the tumors.
Researchers collected tissue specimens first at diagnosis and then again at surgery for evaluation. The iodine group was compared with a placebo group. Only the iodine-taking group showed the antiproliferative and cell death results.
Tagged with: breast cancer, hypothyroidism
Breast Cancer, Tamoxifen, Thyroid & Weight Loss
Posted on Feb 23rd, 2010 by Bird
Birdhttp://thyroid.about.com/library/derry/bl1a.htm
Breast Cancer, Tamoxifen, Thyroid & Weight Loss
... An adequate dose of iodine can be defined as more than 4 mg per day. Lugol's solution is an iodine-in-water solution used by the medical profession for 200 years. One drop (6.5 mg per drop) of Lugol's daily in water, orange juice or milk will gradually eliminate the first phase ofthe cancer development namely fibrocystic disease of the breast so no new cancers can start. It also will kill abnormal cells floating around in the body at remote sites from the original cancer. Of course this approach appears to work for prostate cancer as prostate cancer is similar to breast cancer in many respects. Indeed, it likely will help with most cancers.
http://www.publications.parliament.uk/pa/cm199900/cmselect/cmsctech/332/0062112.htm
INTRODUCTION
As a member of BREAST UK I am a patient advocate. I am a retired biomedical scientist with personal experience of both breast cancer and hypothyroidism. Looking at the research into both diseases, it soon becomes evident that there is a link between all cancers and hypothyroidism.
In fact, if hypothyroidism were taken seriously, not only would much cancer be PREVENTED and outcomes in treatment be improved, but other ailments such as ME and heart disease would also benefit. This would save the NHS a great deal of money in a relatively short time.
The following is an overview of some of the literature illustrating how low thyroid is implicated in cancer, and how equivocal blood test results have let patients down and made some existing research unclear.
The purpose of this memorandum is to bring to your attention the link between hypothyroidism and cancer with the hope that more research will follow, leading to improved patient outcomes.
1. HYPOTHYROIDISM. THE UNSUSPECTED ILLNESS. BY BRODA O BARNES
1.1 This is an old book but it tells how people suffer for years without being properly diagnosed and are then treated with synthetic hormone that doesn't always work. The sin is that it is all still relevant today. His theories are backed with research. He realised that hypothyroidism is associated with atherosclerosis, heart disease, diabetes and cancer.—(Ref:1)
YOUR THYROID BY THE BRODA O BARNES M.D. RESEARCH FOUNDATION INC—(REF 2)
1.2 Every cell in the body needs thyroid hormone, therefore, every cell will feel the effects of deficiency. Which systems develop symptoms first depends on individual strengths and weaknesses.' This sheet explains how the thyroid controls metabolism—the energy needed in every cell to function properly. With lower body temperatures all the enzymes work more sluggishly.
2. LOW RESISTANCE TO DISEASES AND CANCER IS INCREASING IN THE MODERNWORLD
2.1 Broda Barnes's theory is that, whereas low thyroid people would have died from infections, especially TB, with the introduction of antibiotics they were now surviving and reproducing. Hypothyroidism runs in families.
2.2 Richard M Alford MD says that the cause is the failure to treat maternal hypothyroidism during pregnancy. The foetus supplements the maternal deficiency from about the fifth month and the child is born deficient. Like Broda Barnes he attributes many diseases and problems to hypothyroidism. "Those with very poor metabolic function will die very young on average in spite of their genes. The optimal thriving condition in an euthyroid individual increases their capability to suppress the effects of their abnormal genes".— (Ref: 3)
2.3 Environmental hormone disrupters, find their way into our bodies—mimic the shape of the real hormone and block the receptor site.—(Ref: 4)
- "In many instances, specific hormones and the biological processes they control are chemically identical in animals and humans," and "this means that a chemical which affects the same component of the endocrine system of an insect can be expected to similarly affect a mammal".
2.4 The EU Commission is gathering evidence to identify a list of 100 potential endocrine disrupting substances. Report due in April 2000. Particular reference to herbal oestrogens, phthalates used in plastics and pesticides.
2.5 Dr Durrant-Peatfield lists a number of chemical agents that interfere with the manufacture of thyroid hormone. Chemicals in paints & wood preservatives, plastics, some vegetables, cigarette smoke, caffeine, aspirin and fluorides etc. (Fluoride is added to some water supplies!)—(Ref: 5)
2.6 Selenium is a dietary supplement recommended for cancer prevention. Areas of naturally high selenium intake, like Japan, have lower breast cancer mortality. Selenium is a component of the enzyme that is needed to convert Thyroxine T4 into T3 which can then be used by individual cells in the body.—(Ref: 6)
3. MANY STUDIES HAVE SHOWN THAT THERE IS A HIGH INCIDENCE OFHYPOTHYROIDISM IN BREAST CANCER PATIENTS
3.1 Study by the Institutes of Endocrinology and Pathology, University of Pisa, Italy. This study examined breast cancer patients, before starting any therapies, all from an iodine sufficient area. Thyroid disease was present in 46 per cent of breast cancer patients and in 14 per cent of controls. (This was using the less sensitive lab tests!)—(Ref: 7)
3.2 An article in the Lancet in 1974—(Ref: 8).
This study showed that a large number of patients with breast cancer have sub-optimal level of thyroid activity which is not secondary to pituitary or hypothalamic disease. Areas where endemic goitre is uncommon have a low breast cancer mortality and it is increased in areas where it is common. Low thyroid in breast cancer has an adverse effect of prognosis, and thyroidectomy performed on patients with apparently stable breast cancer can cause sudden dissemination of the disease. The above report suggests a causal relationship between thyroid dysfunction and breast cancer.
3.3 Another article in the Lancet in 1974—(Ref: 9).
Hypothesis based on previous experimental evidence that a sub-optimal level of circulating thyroid hormones may abnormally sensitise mammary epithelial cells to prolactin stimulation, leading to dysplasia and eventual neoplasia. It is also possible that with sub-optimal levels of thyroid hormones, prolactin initiates malignant transformation in cells unprimed for mammotrophic stimulation, probably in the presence of optimal concentrations of growth hormone and ovarian steroids. Plasma prolactin levels in patients with early or advanced breast cancer are normal but TSH (Thyroid Stimulating Hormone) is significantly raised.
4. THYROID-PITUITARY FUNCTION AND RESPONSE TO THERAPY
4.1 A study in Japan found that the patients whose disease progressed, showed significantly lower T3 levels and higher TSH, and their tumours were resistant to subsequent therapies. Prolactin levels were higher in the "progressive disease" and "no change" groups compared to "partial response" group.—(Ref: 13).
5. THERAPIES—AETIOLOGY
5.1 A study showing concerns about radiogenic effects of irradiation outside the treated area. It measured the scattered dose to contra-lateral breast, thyroid and gonads.—(Ref: 10).
5.2 Breast cancer patients near Chernobyl, demonstrated significant disturbances in function of hypophyseal-thyroid and hypophyseal-adrenal axes. These may effect prolactin secretion, which worsens the prognosis.—(Ref: 11).
5.3 Hypothyroidism & Tamoxifen
Symptoms are the same as the side effects attributed to Tamoxifen, and cause many people to stop using Tamoxifen. It would be logical to screen all breast cancer patients for hypothyroidism as part of their adjuvant therapy. Perhaps more patients would then stay on the regime or would not suffer these distressing symptoms. Tamoxifen also influences thyroid hormone levels by modulating plasma TBG (thyroid binding globulin) & by interfering with hormone synthesis or secretion in the thyroid gland.—(Ref: 12).
5.4 Low basal temperatures mean that all the hormones are not working at optimal temperature. This must affect the blocking reaction of tamoxifen and oestrogen, rendering it less effective.
6. THYROID FUNCTION TESTING
Dealing with interpretation difficulties.—(Ref: 14)
6.1 Blood tested by the laboratory can only give a snapshot in time. It varies in response to cold or illness. Levels are greater in the early morning and lower in the evening. There is also a day to day cyclical variation.
6.2 The tests:
- — Total T4—measures circulating thyroxine. Does not show how utilised in the body.
- — T3 uptake—is only an estimate of sites not taken up by T4 and has only a 50-60 per cent sensitivity for hypothyroid states.
- — TSH—(Thyroid Stimulating Hormone) measures pituitary response to circulating T3 & T4. A sensitive TSH test is available. There is diurnal variation.
- — Free T4—a better assessment of thyrometabolic rate than total T4.
- — Total T3—the active form of the hormone. More useful to indicate hyperthyroidism as the test is more accurate at the higher levels.
6.3 Thyroid hormone available in the blood stream may not reach proper equilibrium with the extra-cellular fluid and cells. The body will attempt to maintain blood levels within certain ranges no matter what is occurring at the cellular level. Physicians should bear in mind the variables in the time that the sample is taken. Laboratory error and different testing methods add further variations.
6.4 Reference ranges are determined from a wide population. Patients who are marginally ill may fall within the range and so are missed. Lab tests should not be used to make a diagnosis, but to substantiate clinical signs and symptoms. The patients optimal range should be found rather than basing on population studies. Other medications may affect some patients in regulating thyroid supplementation.
6.5 Basal Body Temperature—as advocated by Broda Barnes MD.—(Ref: 1, 2, 5, 14)
A more sensitive indicator of hypothyroidism than blood testing. It gives an indication of what is occurring during optimal thyroid output rather than a random blood draw. It gives a better indication of what is occurring at the cellular level by measuring the body's metabolic response.
June 2000
REFERENCES
1. Hypothyroidism, The Unsuspected Illness. By Broda O Barnes MD and Lawrence Galton. ISBN 0-690-01029-X www.amazon.com—also have reviews.
2. Your Thyroid. Broda O Barnes M.D. Research Foundation Inc. www.my4tune.u-net.com/hypo.html
3. Richard M Alford MD—Low Metabolism or Hypothyroidism.www.valint.net/php/rmalford/
4. Environmental Estrogens. The Endocrine System & Endocrine Disruptor News. How Endocrine Disrupters Work. www.wwfcanada.org/hormone-disruptors/science/endosys.html
5. Article—Suggestions for an approach to the management of thyroid deficiency. Dr Durrant-Peatfield. www.my4tune.u-net.com/appto_treatment.html
6. Article—Richard A Passwater, Ph.D. New discoveries expand our knowledge about selinium's importance.www.healthy.net/hwlibraryarticles/passwater/noninterview/selinium.htm
7. The Journal of Clinical Endocrinology & Metabolism. Vol 81, No. 3, pp. 990-994 March 1996. Study by the Institutes of Endocrinology and Pathology, University of Pisa, Italy.
8. The Lancet 11 May 1974. Hypothalmic-Pituitary-Thyroid axis in Breast Cancer. I Mittra & J L Hayward, Imperial Cancer Research Fund Breast Cancer Unit. Guy's Hospital, London.
9. The Lancet 11 May 1974. Hypothalmic-Pituitary-Prolactin axis in Breast Cancer. I Mittra, J L Hayward, Imperial Cancer Research Fund Breast Cancer Unit, Guy's Hospital & A S McNeilly, St Bartholomew's Hospital, London SE1 9RT
10. Article—An in-vivo dosimetric study of the scattered radiation during the treatment of breast carcinoma. Radiologia Medica 91(1-2):122-5, 1996 Jan-Feb.
11. Article—The functional status of the hypophyseal-thyroid and hypophyseal-adrenal systems in breast cancer patients taking into account their exposure to the factors of the accident at the Chernobyl Atomic Electric Power Station. Likarska Sprava. (5-6); 29-31, 1995 May-June.
12. Article—Thyroid function in post menopausal breast cancer patients treated with Tamoxifen. Scandinavian Journal of Clinical & Laboratory Investigation. 58(2):103-7 April 1998
13. Relationship between thyroid-pituitary function and response to therapy in patients with recurrent breast cancer. 1996 July-August, Gunma University School of Medicine, Japan.
14. Journal of Naturopathic Medicine. Thyroid Function Testing: Dealing with Interpretation Difficulties.www.healthy.net/hwlibraryjournals/naturopathic/vol1no1/thyroid.htm http://www.thyroid-info.com/articles/brownstein-hormones.htm
I agree that iodine can aggravate autoimmune thyroid conditions. Iodine supplementation in those that have an autoimmune thyroid problem can be akin to pouring gas over a fire. However, with hypothyroid conditions that are not autoimmune in nature, iodine-containing foods can actually help the thyroid function better.
3-Week Course of Breast Radiation May Be as Effective as ....
Posted on Feb 23rd, 2010 by Bird
Birdhttp://www.hopkinsbreastcenter.org/artemis/200912/1.html
According to a study presented at the 51st Annual Meeting of the American Society for Radiation Oncology (ASTRO), a shortened, more intensive course of radiation given to the whole breast, along with an extra dose of radiation given to the surgical bed of the tumor (concomitant boost), has been shown to result in excellent local control at a median follow up of two years after treatment with no significant sides effects.
"The observations to date suggest that a three-week course of radiation therapy with concomitant boost results in outcomes comparable to that of a five to seven week course for early stage-breast cancers. Additional studies with a larger body of data and longer follow-up period will help establish whether this type of radiation treatment should be routinely used," Manjeet Chadha, M.D., lead author of the study and a radiation oncologist at the Beth Israel Medical Center in New York said.
This shorter treatment, called accelerated hypofractionated whole breast irradiation, is an especially attractive option because women can receive a full course of radiation therapy in half the time – three weeks of daily treatments vs. five to seven weeks. In addition, the cost of this treatment is lower relative to the cost of the standard whole breast radiation and is also less expensive than other new approaches, such as partial breast irradiation (breast brachytherapy).
"Studies from Europe and Canada have used accelerated schedules for breast radiation therapy with favorable results reported on longer follow up. In the U.S., however, there is limited data on this topic," Chadha said. "Additionally, the radiation therapy technique used in our study is different from previously published experiences. For each patient, we developed a conformal, personalized plan using three-dimensional dosimetry data derived from the patient specific CT scan images. Radiation treatment was delivered to the whole breast using an accelerated hypofractionated schedule, with the simultaneous delivery of a boost dose given to the precise location from which the tumor was removed."
Many women with early-stage breast cancer undergo breast conserving therapy. Typically, this means they first have surgery to remove the visible cancer (a lumpectomy), and then receive a course of radiation therapy to kill any microscopic cancer cells that may remain. The standard whole breast radiation treatment takes 15 to 30 minutes every day, Monday through Friday, for five to seven weeks.
Beginning in June 2004, researchers studied 112 women with early-stage breast cancer who received accelerated hypofractionated whole breast irradiation plus concomitant boost. The results were reported on 105 patients who had completed therapy and had a minimum six-month follow up. The patient group had small breast tumors that had not spread to the lymph nodes. Women with early-stage breast cancer who received chemotherapy or underwent radiation to the lymph nodes were excluded from the study. Patients were followed at regular intervals after completion of treatment.
Findings show that the cancer did not return to the original site or to the surrounding region in these women. The median follow-up of the study was two years. Survival was greater than 95 percent for patients with five years of follow up. The study also shows there were no significant physical or cosmetic side effects from the radiation treatment.
In an era of personalized care, Chadha emphasizes, "Women with early-stage breast cancer interested in this shorter course should ask their radiation oncologists about this option to evaluate whether it is suitable for their individual case."
SOURCES:
51st Annual Meeting of the American Society for Radiation Oncology, November 4, 2009, Chicago, IL
American Society for Radiation Oncology (http://www.astro.org
51st Annual Meeting of the American Society for Radiation Oncology, November 4, 2009, Chicago, IL
American Society for Radiation Oncology (http://www.astro.org
Tagged with: breast cancer
CoQ10 and metastases
Posted on Feb 20th, 2010 by Bird
Birdhttp://www.ncbi.nlm.nih.gov/pubmed/16443053
http://www.cancer.gov/cancertopics/pdq/cam/coenzymeQ10/HealthProfessional/page6
http://www.ncbi.nlm.nih.gov/pubmed/18407793?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1
also
http://www.sciencedirect.com.proxy.lib.siu.edu/science?_ob=ArticleURL&_udi=B6X3P-4S08JWP-1&_user=1412102&_coverDate=06%2F30%2F2008&_alid=1214534360&_rdoc=29&_fmt=high&_orig=search&_cdi=7304&_sort=r&_docanchor=&view=c&_ct=167&_acct=C000052645&_version=1&_urlVersion=0&_userid=1412102&md5=a3c2053544e22a8cd677bd4bb2cc0a78
J Am Acad Dermatol. 2006 Feb;54(2):234-41. Epub 2005 Dec 27.
Low plasma coenzyme Q10 levels as an independent prognostic factor for melanoma progression.
Rusciani L, Proietti I, Rusciani A, Paradisi A, Sbordoni G, Alfano C, Panunzi S, De Gaetano A, Lippa S.
Department of Dermatology, Catholic University of the Sacred Heart, Rome, Italy.
BACKGROUND: Abnormally low plasma levels of coenzyme Q10 (CoQ10) have been found in patients with cancer of the breast, lung, or pancreas. OBJECTIVE: A prospective study of patients with melanoma was conducted to assess the usefulness of CoQ10 plasma levels in predicting the risk of metastasis and the duration of the metastasis-free interval. METHODS: Between January 1997 and August 2004, plasma CoQ10 levels were measured with high-performance liquid chromatography in 117 consecutive melanoma patients without clinical or instrumental evidence of metastasis according to American Joint Committee on Cancer criteria and in 125 matched volunteers without clinically suspect pigmented lesions. Patients taking CoQ10 or cholesterol-lowering medications and those with a diagnosis of diabetes mellitus were excluded from the study. Multiple statistical methods were used to evaluate differences between patients and control subjects and between patients who did (32.5%) and did not (67.5%) develop metastases during follow-up. RESULTS: CoQ10 levels were significantly lower in patients than in control subjects (t test: P < .0001) and in patients who developed metastases than in the metastasis-free subgroup (t test: P < .0001). Logistic regression analysis indicated that plasma CoQ10 levels were a significant predictor of metastasis (P = .0013). The odds ratio for metastatic disease in patients with CoQ10 levels that were less than 0.6 mg/L (the low-end value of the range measured in a normal population) was 7.9, and the metastasis-free interval was almost double in patients with CoQ10 levels 0.6 mg/L or higher (Kaplan-Meier analysis: P < .001). LIMITATIONS: A study with a larger sample, which is currently being recruited, and a longer follow-up will doubtlessly increase the statistical power and enable survival statistics to be obtained. CONCLUSIONS: Analysis of our findings suggests that baseline plasma CoQ10 levels are a powerful and independent prognostic factor that can be used to estimate the risk for melanoma progression.
Vascul Pharmacol. 2008 Apr-Jun;48(4-6):191-201. Epub 2008 Mar 5.
Anti-angiogenic potential of CoenzymeQ10, riboflavin and niacin in breast cancer patients undergoing tamoxifen therapy.
Department of Medical Biochemistry, DR. A.L.M. Post-Graduate, Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai, India.
Tumour angiogenesis is a complex mechanism consisting of multi-step events including secretion or activation of angiogenic factors by tumour cells, activation of proteolytic enzymes, proliferation, migration and differentiation of endothelial cells. Both primary and metastatic tumours in the breast are dependent on angiogenesis. In the present study, 84 breast cancer patients were randomized to receive a daily supplement of CoQ(10) 100 mg, riboflavin 10 mg and niacin 50 mg (CoRN), one dosage per day along with tamoxifen (TAM) 10 mg twice a day. Serum pro-angiogenic levels were elevated in untreated breast cancer patients (Group II) and their levels were found to be reduced in breast cancer patients undergoing TAM therapy for more than 1 year (Group III). When these group III breast cancer patients were supplemented with CoRN for 45 days (Group IV) and 90 days (Group V) along with TAM, a further significant reduction in pro-angiogenic marker levels were observed. Supplementing CoRN to breast cancer patients has found to decrease the levels of pro-angiogenic factors and increase the levels of anti-angiogenic factors. A reduction in pro-angiogenic marker levels attributes to reduction in tumour burden and may suggest good prognosis and efficacy of the treatment, and might even offer protection from cancer metastases and recurrence.
http://www.ncbi.nlm.nih.gov/pubmed/18407793?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1
also
http://www.sciencedirect.com.proxy.lib.siu.edu/science?_ob=ArticleURL&_udi=B6X3P-4S08JWP-1&_user=1412102&_coverDate=06%2F30%2F2008&_alid=1214534360&_rdoc=29&_fmt=high&_orig=search&_cdi=7304&_sort=r&_docanchor=&view=c&_ct=167&_acct=C000052645&_version=1&_urlVersion=0&_userid=1412102&md5=a3c2053544e22a8cd677bd4bb2cc0a78
Clin Exp Metastasis. 2008;25(2):161-9. Epub 2007 Dec 5.
Reversing mitochondrial dysfunction, fatigue and the adverse effects of chemotherapy of metastatic disease by molecular replacement therapy.
Department of Molecular Pathology, The Institute for Molecular Medicine, P.O. Box 9355, Laguna Beach, CA 92652, USA. gnicolson@immed.org
Metastatic cancers are associated with cellular oxidative stress, and during cancer chemotherapy excess drug-induced oxidative stress can limit therapeutic effectiveness and cause a number of side effects, including fatigue, nausea, vomiting, diarrhea and more serious adverse effects, such as cardiomyopathy, peripheral neuropathy, hepatotoxicity and pulmonary fibrosis. We review here the hypothesis that the acute and chronic adverse effects of cancer chemotherapy can be reduced by molecular replacement of membrane lipids and enzymatic cofactors, such as coenzyme Q(10). By administering nutritional supplements with replacement molecules and antioxidants, oxidative membrane damage and reductions of cofactors in normal tissues can be reversed, protecting and restoring mitochondrial and other cellular functions and reducing chemotherapy adverse effects. Recent clinical trials using cancer and non-cancer patients with chronic fatigue have shown the benefit of molecular replacement plus antioxidants in reducing the damage to mitochondrial membranes, restoring mitochondrial electron transport function, reducing fatigue and protecting cellular structures and enzymes from oxidative damage. Molecular replacement and antioxidant administration mitigates the damage to normal tissues, such as cardiac tissue, and reduces the adverse effects of cancer therapy without reduction in therapeutic results.
(Ubiquinone)
The OSL risk assessment method indicates that the evidence of safety is strong at intakes up to 1200 mg/day, and this level is identified as the OSL. Much higher levels have been tested without adverse effects and may be safe, but the data for intakes above 1200 mg/day are not sufficient for a confident conclusion of safety.
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