Iodine, a mineral found in foods, is used by our body to produce thyroid hormones. These hormones regulate the body’s metabolism as well as a variety of other vital functions. Iodine is a necessary component of human physiology. Its role in thyroid function is well understood and heavily emphasized in the literature. Its potential role as an anticarcinogenic agent is only now becoming recognized. Iodine’s molecular effects and ongoing epidemiological evidence suggest that it may play a role in cancer prevention via antioxidant, antiinflammatory, differentiating, and proapoptotic effects. It is especially true for stomach and breast cancers, but it may also be true for many other cancers that have yet to be thoroughly researched. Thyroid hormones are critical players in average growth, development and metabolism, and During pregnancy and infancy, the bones and brain develop. They play a role in the development of some types of human cancer.
How does the thyroid gland function?
The thyroid gland is an essential hormone gland regulating metabolism, growth, and development in the human body. It aids in regulating many bodily functions by continuously releasing a consistent amount of thyroid hormones into the bloodstream. When the body requires more energy in certain situations – for example, growing, cold, or pregnant – the thyroid gland produces more hormones.1(How Does the Thyroid Gland Work?, 2018).This organ (medical term: glandular thyreoidea) is located at the front of the neck, beneath the voice box. It is butterfly-shaped, with two side lobes lying against and around the windpipe (trachea) and are joined at the front by a narrow strip of tissue. On average, the thyroid weighs between 20 and 60 grams. It is encased in two fibrous capsules. The voice box muscles and numerous essential vessels and nerves are all connected to the outer capsule. Because there is a gap between the inner and external capsules, the thyroid can move and change position when we swallow. The thyroid tissue is made up of many small individual lobules surrounded by thin layers of connective tissue. These lobules contain many small cysts (sacs) known as follicles that store thyroid hormones in the form of tiny droplets.
Hormone Production in thyroid
The thyroid gland produces three essential hormones: Tetraiodothyronine, called thyroxine or T4, Triiodothyronine, also known as T3 and calcitonin. Iodine is a critical component of both hormones. Because our bodies are unable to produce this trace element, we must obtain it through our diet. Iodine is absorbed into our bloodstream through our bowels from food. It is then transported to the thyroid gland, where it is eventually converted into thyroid hormones. The bodies require m thyroid hormones at times and less at others. The thyroid gland requires the assistance of another gland, the pituitary gland, to produce the correct amount of hormones. The pituitary gland instructs thyroid gland what to do. release more or fewer hormones into the bloodstream. In addition, a small amount of thyroid hormone is attached to blood transport proteins.
An overactive thyroid (also referred to as hyperthyroidism) occurs when the thyroid gland produces excessive hormones. The thyroid gland produces insufficient hormones. When it is underactive (hypothyroidism). Both of these imbalances have the potential to cause a wide range of symptoms. Hypothalamic thyrotropin-releasing hormone (TRH) stimulates the pituitary gland to synthesize and secrete thyroid-stimulating hormone (TSH) stimulate. TH synthesis and secretion at the thyroid gland. The primary hormone synthesized in the thyroid gland, tetraiodothyronine (T4), is catalyzed to triiodothyronine (T3) by specific iodothyronine deiodinases2.(Piekiełko-Witkowska & Nauman, 2011)T3 is the direct TH that mediates metabolic activity through the formation of complexes between T3 and the nuclear thyroid hormone receptors alpha (TR) and beta (TR). This nuclear T3-receptor complex binds to thyroid hormone response elements on specific genes, controlling transcription. Diseases caused by an excess of TH (hyperthyroidism) or a lack of TH (hypothyroidism) are common and preventable3(Krashin et al., 2019). It was hypothesized that TH deficiency could influence cancer outcome. Numerous clinical studies have supported this assumption, demonstrating that hypothyroidism inhibits tumour growth while hyperthyroidism has the opposite effect (6). Thyroid hormones have been studied in recent decades to see how they promote the growth of cancer cells.
Thyroid hormones and Cancer
Thyroid hormones can influence Cancer or can increase the risk of developing Cancer. The chances of Cancer and prostate cancer increase due to low TSH levels. Elevated TSH levels are associated with excellent progression-free survival in a small study of breast cancer patients. Clinical studies indicate that thyroid cancer patients undergoing I treatment have an increased incidence of developing secondary malignancies of the breast and stomach; it has also been reported that Serum and urinary iodine levels are significantly higher in patients with gastric cancer, especially in the late stage. For decades, research has suggested that some breast diseases may be classified as iodine deficiency diseases. The following evidence supports this hypothesis: 1) Iodine-rich seaweed has an anti-cancer effect on breast cancer cells and animal models incorporating seaweed into rats’ diets delays the onset and number of rat mammary tumours Iodine improved symptoms in women with the fibrocystic disease who had painful breasts , and 4) iodine consumption in the United States has dropped by half since the 1970s as breast cancer rates have risen. On the other hand, Japanese women consume 25 times more dietary iodine than North American women and have lower breast cancer rates. Thyroid cancer risk increased by 31%–73% after breast cancer, and breast cancer risk increased by 21%–89% after thyroid cancer . Furthermore, breast cancer was three times more likely in thyroid cancer patients aged 40–50 years than in age-matched controls . Moreover, studies show that the incidence of Cancer, particularly Cancer of the breast and stomach, is higher in patients treated with radioactive Iodine (RAI) as first-line therapy for hyperthyroidism.
1.Increased cancer risk in general
2.Thyroid cancer risk is increased.
3.Some studies found an increase in cancer mortality and a decrease in five- and ten-year survival, while others found no link.
4.Subclinical and clinical hyperthyroidism raises the risk of a variety of solid tumours.
5.It is linked to an increased risk of colorectal Cancer.
Hypothyroidism (underactive thyroid)
1.More significant Cancer (advanced neoplasms of melanoma, renal cell carcinoma, lymphoma and colon cancer) were treated with interleukin-2 and lymphokine-activated killer (LAK) cells.
2.Increased aggressiveness of colorectal and liver Cancer
3.Higher risk of thyroid cancer
4.Breast cancer role is inconclusive, with different analyses finding opposite trends.
5.May reduce the aggressiveness of, or delay onset of, Cancer
6.Associated with increased risk of colorectal Cancer (untreated hypothyroidism)
7.When compared to breast cancer patients without thyroid disease, Thyroid disease, particularly hypothyroidism, was associated with a significantly lower incidence of lymph node metastases
Molecular Iodine attacks breast Cancer.
Iodine supplementation has been shown to improve breast health, but no one has determined how it works with FBC cells. The researchers wanted to find the specific MOA that made molecular Iodine effective. Although molecular Iodine can promote breast health and protect women from fibrocystic breast disease and potentially cancer, no one has ever identified the molecular iodine mechanism in fibrocystic breast disease. In vitro studies were carried out to assess the biochemical interaction that molecular Iodine has been shown to interact with breast cancer cells and cells derived from fibrocystic breast tissue. In vitro studies were carried out to determine the biochemical interaction that molecular Iodine has with Cells derived from fibrocystic breast tissue and breast cancer cells MCF10A is a human immortalized mammary epithelial cell line derived from the fibrocystic breast tissues of a 36-year-old Caucasian female., was used in the FBC study. It was given various doses of molecular Iodine, and its proliferation was measured. The ages). Cells were treated with varying concentrations of molecular Iodine to assess proliferation and cell death apoptosis. Following that, gene expression analysis of critical molecular markers, primarily responsible for cell growth and apoptosis, was performed. As an internal control, primary human mammary epithelial cells derived from a healthy female donor were used. According to the findings of these studies, molecular Iodine has potent inhibitory effects on cell growth in both breast cancer and FBC. Gene expression analysis using quantitative RT-PCR in the FBC study confirmed that cell cycle genes controlling the G1-S phase transition were upregulated. Cyclin B expression levels did not change significantly, indicating that cells were arrested before entering cell division6. The expression of the nuclear hormone receptors PPAR- and PPAR- was increased. BCL-2, a cell death inhibitor, was upregulated while caspase-3 expression was downregulated, implying that molecular Iodine can cause cell death via caspase-independent apoptosis.
Food and Iodine
A diet lacking in Iodine and other essential nutrients can contribute to thyroid-related illnesses, including Cancer. Iodine-rich foods include fish (including cod and tuna), seaweed, shrimp, and other seafood. Dairy products and grain products (such as bread and cereals) are the primary sources of Iodine in American diets. Fruits and vegetables contain Iodine, though the amount varies depending on the iodine content of the soil in which they were grown, and any fertilizer used. Iodized salt is widely available in the United States and many other countries; however, processed foods like canned soups rarely contain iodized salt4(“How Molecular Iodine Attacks Breast Cancer,” 2016). Foods are rich in zinc and vitamins A and E, such as chicken, peas, fish, and vegetables, aid in the proper production of thyroid hormones.
Other foods can interfere with the body’s ability to use Iodine. Those who have thyroid cancer or are at high risk of developing thyroid cancer should avoid the following foods: cabbages, soy, and cassava.
Iodine and Breast Cancer
A renewed search for a link between breast cancer and thyroid disease has revealed an increased prevalence of autoimmune thyroid disease in breast cancer patients. The relatively low rate of breast cancer in Japanese women who consume a diet rich in iodine-rich seaweed backs up experimental findings that iodine or iodine-rich seaweed can inhibit breast tumour development. However, no direct evidence exists that Iodine, iodinated compounds, or a combination of Iodine and selenium are the anti mammary carcinogenic element8(Goldman, 1990). It is a link with the alleged link between breast cancer and thyroid disorders. Because both breast cancer and thyroid disease primarily affect women and have a postmenopausal peak incidence, there has inevitably been a search for a link between the two conditions9(Smyth, 2003). There is an association between breast cancer and hyperthyroidism and hypothyroidism. Hypothyroidism was the most commonly observed finding when a connection between thyroid disease and breast cancer was discovered. Many studies considered hyperthyroidism to be protective against breast cancer because the progression of such cancers was more common when hyperthyroidism was treated. The possibility that hypothyroidism may have been beneficial in terms of breast cancer outcome has been raised . Recent findings from our laboratory  show that the presence of TPO antibodies is associated with a significant improvement in both disease-free and overall outcome in breast cancer patients. The magnitude of this prognostic effect was comparable to that of a placebo effect.
In iodine deficiency, chronic TSH stimulation
Normal thyroid follicular cells proliferate slowly, but in iodine-deficient animals, serum TSH rises, and thyroid cell proliferation rates increase 5 to 30-fold. But in iodine-deficient animals, TSH levels rise, and thyroid cell proliferation rates increase by 5 to 30-fold, resulting in marked thyroid hyperplasia and hypertrophy. Rapidly proliferating thyrocytes are more likely to be vulnerable to mutagens such as radiation, chemical carcinogens, and oxidative stress, and they may accumulate a greater number of genetic alterations. Thyroid hyperplasia caused by iodine deficiency causes chromosomal changes in the rat thyroid, resulting in an increase in the number of aneuploid cells. Several authors have suggested that thyroid tumours iodine deficiency is caused by chronic TSH overstimulation, which may collaborate with epidermal growth factor and insulin-like growth factor I. Chronic TSH stimulation induced by goitrogen-containing diets or partial thyroidectomy has been shown in rat studies to be consistent with this hypothesis. Results in a transition from thyroid follicular adenomas to follicular carcinomas. This hypothesis is also consistent with increased FTC and ATC findings in populations with severe endemic goitre because serum TSH is increased in moderate-to-severe iodine deficiency to maintain euthyroidism.
Iodine, oxidative damage and apoptosis
Other mechanisms, in addition to chronic TSH stimulation, may play a role in thyroid tumorigenesis during iodine deficiency. Iodine deficiency increases the production of H2O2-mediated reactive oxygen species (ROS), which damages DNA and causes mutations. (Zimmermann & Galetti, 2015). The activity of antioxidant enzyme systems, including superoxide dismutase-3, is increased in iodine-deficient rat thyroids. This is accompanied by increased uracil and oxidized purine or pyrimidine adducts thyroid DNA. Excess molecular iodide, produced by the oxidation of Iodine by endogenous peroxidases, induces apoptosis in immortalized thyroid cell cultures (TAD-2) and primary cultures of human thyroid cells via a mechanism involving the generation of free radicals. Giving extra iodide to human thyroid cell lines reduces H2O2 production. Through the ages of iodolactones, Iodine exposure can also cause apoptosis in human thyroid cells and thyroid carcinoma cell lines (iodinated derivatives of fatty acids)
Gastric carcinoma is said to be more common in areas where diets are either iodine-deficient or iodine-excessive. According to reports, there has also been an increase—the link between thyroid diseases and a few of the risk factors for Gastric Cancer. The researchers compared the frequency of thyroid disorders in 61 patients with gastric carcinoma to 55 healthy controls subjects under control. Thyroid health was examined—Physical examination and evaluation by determining thyroid serum levels, thyroid autoantibodies, and hormones. Compared to healthy controls, more patients with gastric Cancer had goitre (49.1 per cent versus 20 per cent, respectively). There has still been a significant increase in the number of patients diagnosed with gastric cancer. There was also a substantial difference in the prevalence of autoimmune thyroid disease: 27.8 per cent of patients with gastric Cancer were affected, compared to 10.9 per cent of control subjects. These findings suggest a link between gastric Cancer and thyroid problems8(Kandemir et al., 2005)(Zimmermann & Galetti, 2015).
Iodine can interact with many medications. Before taking an iodine supplement, consult a physician regarding safe use. Consult a pharmacist to check to take any medications or supplements that may interact with Iodine. Excessive iodine consumption can be harmful to one’s health (hyperthyroidism, goitre, thyroiditis, thyroid cancer). An overdose can cause acute poisoning symptoms. When taking iodine doses considered safe for the general population, people with autoimmune thyroid disease and iodine deficiency may experience side effects. Excessive iodine consumption can be harmful to one’s health (hyperthyroidism, goitre, thyroiditis, thyroid cancer). An overdose can cause acute poisoning symptoms. When taking iodine doses considered safe for the general population, people with autoimmune thyroid disease and iodine deficiency may experience side effects. Some people are intolerant or sensitive to Iodine, which can be found in chemical agents such as radiocontrast agents (for x-rays), iodine-containing disinfectants such as Betadine, or even foods. If a person suspects they have an iodine allergy, their doctor can conduct tests to confirm the diagnosis. Before receiving medical treatment, an individual should ensure that all medical professionals know an iodine allergy5. Treatment with radioactive Iodine (RAI) for thyroid cancer patients does not appear to increase the risk or recurrence of breast cancer6(Zimmermann & Galetti, 2015). Concerning the breast cancer risk associated with RAI therapy, it has also been suggested that childhood exposure to ionizing radiation may increase the risk of this malignancy. Breast cancer risk was approximately 2.4 times higher in women who had previously received RAI for thyroid cancer than those who did not receive this therapy. Furthermore, breast cancer is becoming more common in patients with thyroid cancer, or other thyroid diseasesNuclear Accidents can cause the release of radioactive Iodine into the environment, increasing the risk of thyroid cancer in people exposed to radioactive Iodine, particularly children. People with iodine deficiency who are exposed to radioactive Iodine are at a higher risk of developing thyroid cancer. The Food and Drug Administration in the United States has approved potassium iodide as a thyroid-blocking agent.
To summarise this, all cancers’ aetiology is multifactorial, reducing modifiable risk factors assumed to be beneficial. There is strong evidence that iodine deficiency is a modifiable risk factor for stomach and breast cancer. Thyroid hormones require Iodine to be produced. Recent epidemiologic studies, however, have revealed that breast cancer patients are at an increased risk of developing thyroid cancer and vice versa. This study discovered that Iodine stimulated the transcriptional activity of oestrogen receptor- (ER-) in breast cancer cells. Iodine stimulated the expression of several ER-regulated genes, PS2, Cathepsin D, CyclinD1, Cathepsin D, and PR, both in vitro and in nude mice, which is consistent with its stimulation of both anchorage-dependent and -independent growth of fibroblasts.f ER-positive breast cancer cells and the effect to dampen tumour shrinkage of MCF-7 xenograft in ovariectomized nude mice. These animal studies suggest that iodine deficiency is primarily a promoter of thyroid carcinogenesis rather than an initiator or a complete weak carcinogen. Iodine excess appears to be a soft supporter rather than an initiator. The relevance of the thyroid tumours The relevance of the results of these animal experiments to human lesions is debatable: most of the studies induced severe iodine deficiency and excess, both of which are more severe than in human diets, and the follicular tumours, in general, show a pattern of morphology and behaviour distinct from human thyroid cancers. Tumours show a pattern of morphology and behaviour different from human thyroid cancers (Takatani et al., 1989) (Zenonco.io, 2020)
Anticancer lifestyle, .io, Zenonco retreived from: https://zenonco.io/anti-cancer-lifestyle
Key words: Cancer prevention,Thyroid gland,hormones,hypothyroidism and hyperthyriodism,Molecular iodine,Breast cancer, apoptosis,Gastric carcinoma.
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2How does the thyroid gland work? (2018). https://www.ncbi.nlm.nih.gov/books/NBK279388/
How Molecular Iodine Attacks Breast Cancer. (2016). Oncology Times, 38(24), 34–34. https://doi.org/10.1097/01.cot.0000511599.52147.f1
3Kandemir, E., Yonem, A., & Narin, Y. (2005). Gastric Carcinoma and Thyroid Status. In The Journal of International Medical Research (Vol. 33).
4Krashin, E., Piekiełko-Witkowska, A., Ellis, M., & Ashur-Fabian, O. (2019). Thyroid hormones and cancer: A comprehensive review of preclinical and clinical studies. Frontiers in Endocrinology, 10(FEB). https://doi.org/10.3389/fendo.2019.00059
5Piekiełko-Witkowska, A., & Nauman, A. (2011). Iodothyronine deiodinases and cancer. In Journal of Endocrinological Investigation (Vol. 34, Issue 9, pp. 716–728). Springer. https://doi.org/10.3275/7754
6Smyth, P. P. A. (2003). The thyroid, iodine and breast cancer. Breast Cancer Research, 5(5), 235–238. https://doi.org/10.1186/bcr6387Zimmermann, M. B., & Galetti, V. (2015). Iodine intake as a risk factor for thyroid cancer: A comprehensive review of animal and human studies. Thyroid Research, 8(1), 1–21. https://doi.org/10.1186/s13044-015-0020-8