S<scp>ection of</scp> B<scp>iological and</scp> M<scp>edical</scp> S<scp>ciences</scp>: IODINE METABOLISM AND BREAST CANCER*,†

Eskin, Bernard A.

doi:10.1111/j.2164-0947.1970.tb02988.x

Cited by 67 publications

(3 citation statements)

References 27 publications

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“…1. 4 Recently, it was reported that Japanese women with Hashimoto's thyroiditis have a relatively high risk of breast cancer.…”

mentioning

confidence: 99%

Plasma thyroid-stimulating hormone and thyroxine concentrations in breast cancer

Rose¹,

Davis

1978

Cancer

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Plasma TSH and thyroxine levels were measured in 74 early breast cancer patients and 53 with advanced disease, 77 patients with cancer arising in other organs and 67 healthy women of similar age. The mean plasma TSH levels were higher in the breast cancer cases than the other two groups; the difference was statistically significant only in those with advanced disease. Twelve percent of the early breast cancer and 15% of the advanced breast cancer patients had elevated plasma TSH concentrations, compared with only 1% of the other cancer patients and 3% of the controls. Four breast cancer patients with plasma TSH levels above 85 microIU/ml had subnormal plasma thyroxine levels. Five of 29 (17%) early breast cancer patients had excessive plasma TSH responses to TRH.

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“…1. 4 Recently, it was reported that Japanese women with Hashimoto's thyroiditis have a relatively high risk of breast cancer.…”

mentioning

confidence: 99%

Plasma thyroid-stimulating hormone and thyroxine concentrations in breast cancer

Rose¹,

Davis

1978

Cancer

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“…The cause-effect relationship between iodine deficiency, impaired function of the thyroid gland, and breast cancer has been observed for over 100 years [23][24][25]. Iodine is absorbed via sodium/iodide symporter in the glandular breast tissue, and its role is to promote the growth of the normal tissue [26].…”

Section: Iodine Deficiency and Breast Cancermentioning

confidence: 99%

Is There an Ideal Diet to Protect against Iodine Deficiency?

et al. 2021

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Iodine deficiency is a global issue and affects around 2 billion people worldwide, with pregnant women as a high-risk group. Iodine-deficiency prevention began in the 20th century and started with global salt iodination programmes, which aimed to improve the iodine intake status globally. Although it resulted in the effective eradication of the endemic goitre, it seems that salt iodination did not resolve all the issues. Currently, it is recommended to limit the consumption of salt, which is the main source of iodine, as a preventive measure of non-communicable diseases, such as hypertension or cancer the prevalence of which is increasing. In spite of the fact that there are other sources of iodine, such as fish, seafood, dairy products, water, and vegetables, the high consumption of processed food with a high content of unionised salt, alternative diets or limited salt intake can still lead to iodine deficiency. Thus, iodine deficiency remains a relevant issue, with new, preventive solutions necessary. However, it appears that there is no diet which would fully cover the iodine requirements, and iodine food supplementation is still required.

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“…In addition to the biological actions of iodine in regulating thyroid hormones, iodine has many additional functions, including anti-inflammatory [280,281,282,283], antioxidant [284,285,286,287] and anti-microbial defence [288,289,290,291,292,293,294]. Iodine deficiency has been reported to be associated with increased cancer risk [295] including; breast [286,296,297,298,299], thyroid [300,301,302,303,304,305,306], and prostate cancer [307,308]. Furthermore, iodine has been found to inhibit the carcinogenic process in breast and prostate cancer cell lines [309,310,311,312].…”

Section: Additional Perspectivesmentioning

confidence: 99%

Fluoride Exposure Induces Inhibition of Sodium/Iodide Symporter (NIS) Contributing to Impaired Iodine Absorption and Iodine Deficiency: Molecular Mechanisms of Inhibition and Implications for Public Health

Waugh¹

2019

IJERPH

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The sodium iodide symporter (NIS) is the plasma membrane glycoprotein that mediates active iodide transport in the thyroid and other tissues, such as the salivary, gastric mucosa, rectal mucosa, bronchial mucosa, placenta and mammary glands. In the thyroid, NIS mediates the uptake and accumulation of iodine and its activity is crucial for the development of the central nervous system and disease prevention. Since the discovery of NIS in 1996, research has further shown that NIS functionality and iodine transport is dependent on the activity of the sodium potassium activated adenosine 5′-triphosphatase pump (Na+, K+-ATPase). In this article, I review the molecular mechanisms by which F inhibits NIS expression and functionality which in turn contributes to impaired iodide absorption, diminished iodide-concentrating ability and iodine deficiency disorders. I discuss how NIS expression and activity is inhibited by thyroglobulin (Tg), tumour necrosis factor alpha (TNF-α), transforming growth factor beta 1 (TGF-β1), interleukin 6 (IL-6) and Interleukin 1 beta (IL-1β), interferon-γ (IFN-γ), insulin like growth factor 1 (IGF-1) and phosphoinositide 3-kinase (PI3K) and how fluoride upregulates expression and activity of these biomarkers. I further describe the crucial role of prolactin and megalin in regulation of NIS expression and iodine homeostasis and the effect of fluoride in down regulating prolactin and megalin expression. Among many other issues, I discuss the potential conflict between public health policies such as water fluoridation and its contribution to iodine deficiency, neurodevelopmental and pathological disorders. Further studies are warranted to examine these associations.

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Section of Biological and Medical Sciences: IODINE METABOLISM AND BREAST CANCER*,†

Cited by 67 publications

References 27 publications

Plasma thyroid-stimulating hormone and thyroxine concentrations in breast cancer

Plasma thyroid-stimulating hormone and thyroxine concentrations in breast cancer

Is There an Ideal Diet to Protect against Iodine Deficiency?

Fluoride Exposure Induces Inhibition of Sodium/Iodide Symporter (NIS) Contributing to Impaired Iodine Absorption and Iodine Deficiency: Molecular Mechanisms of Inhibition and Implications for Public Health

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