Cabbage and thyroid. 9 Foods to Avoid with Hypothyroidism: Thyroid-Friendly Diet Guide
What foods should you avoid if you have hypothyroidism. How does diet affect thyroid function. Which nutrients are important for thyroid health. What are the best dietary choices for managing hypothyroidism.
Understanding Hypothyroidism and Its Dietary Impacts
Hypothyroidism is a common endocrine disorder affecting millions worldwide. It occurs when the thyroid gland doesn’t produce enough thyroid hormones, leading to a slowdown of various bodily functions. While medication is the primary treatment, diet plays a crucial role in managing the condition.
Certain foods can interfere with thyroid function or medication absorption, making it essential for those with hypothyroidism to be mindful of their dietary choices. Let’s explore the foods to avoid and why they may be problematic for individuals with an underactive thyroid.
Cruciferous Vegetables: A Double-Edged Sword
Cruciferous vegetables, such as cabbage, broccoli, and kale, are often touted for their health benefits. However, for those with hypothyroidism, these vegetables can be problematic. Why? They contain goitrogens, substances that can interfere with thyroid hormone production.
Goitrogens can block the thyroid’s ability to absorb iodine, a crucial nutrient for thyroid function. Does this mean you should completely avoid these nutritious vegetables? Not necessarily. Cooking cruciferous vegetables can reduce their goitrogenic properties, making them safer for consumption in moderation.
Balancing Cruciferous Vegetables in Your Diet
- Cook cruciferous vegetables thoroughly to reduce goitrogen content
- Limit intake to 1-2 servings per week
- Consider consuming them with iodine-rich foods to offset potential effects
Soy Products: Potential Thyroid Disruptors
Soy and soy-based products have gained popularity as health foods, but they can be problematic for individuals with hypothyroidism. Soy contains isoflavones, compounds that can interfere with thyroid hormone synthesis and potentially worsen hypothyroidism.
Additionally, soy may interfere with the absorption of thyroid medication. If you’re taking thyroid hormone replacement therapy, it’s crucial to be cautious with soy consumption. How can you safely include soy in your diet if you have hypothyroidism?
Managing Soy Intake with Hypothyroidism
- Limit soy consumption to small amounts
- Avoid consuming soy products within 4 hours of taking thyroid medication
- Choose fermented soy products, which may be less problematic
- Consult with your healthcare provider about your individual soy tolerance
Gluten: A Potential Trigger for Thyroid Issues
For some individuals with hypothyroidism, particularly those with autoimmune thyroid conditions like Hashimoto’s thyroiditis, gluten can be problematic. Gluten is a protein found in wheat, barley, and rye. Some studies suggest a link between gluten sensitivity and autoimmune thyroid disorders.
Why might gluten be an issue for thyroid health? The molecular structure of gluten closely resembles that of thyroid tissue. In susceptible individuals, this similarity can trigger an immune response that may exacerbate thyroid problems.
Considering a Gluten-Free Diet
- Consult with a healthcare provider before eliminating gluten
- Try a gluten-free diet for several weeks to see if symptoms improve
- Be aware of potential nutrient deficiencies when avoiding gluten-containing foods
- Choose naturally gluten-free grains like quinoa, rice, and millet
Excessive Iodine: Too Much of a Good Thing
Iodine is essential for thyroid function, but excessive intake can be harmful, especially for those with hypothyroidism. High iodine consumption can exacerbate thyroid problems and interfere with thyroid hormone production.
Foods high in iodine include seaweed, kelp supplements, and some iodized salt. While iodine deficiency is rare in developed countries due to iodized salt, overconsumption can occur through supplements or certain foods.
Balancing Iodine Intake
- Avoid kelp and seaweed supplements unless recommended by a healthcare provider
- Use iodized salt in moderation
- Be cautious with foods high in added iodine
- Consult your doctor about your individual iodine needs
Processed Foods: Hidden Thyroid Disruptors
Processed foods often contain additives and preservatives that can interfere with thyroid function. These foods are typically high in sodium, which can lead to fluid retention and exacerbate symptoms of hypothyroidism. Moreover, they often lack the nutrients essential for optimal thyroid health.
Many processed foods also contain trans fats and refined sugars, which can contribute to inflammation and potentially worsen thyroid problems. How can you reduce processed foods in your diet?
Minimizing Processed Foods
- Focus on whole, unprocessed foods
- Read labels carefully to avoid hidden additives
- Cook meals from scratch using fresh ingredients
- Choose healthier alternatives to processed snacks
Caffeine: A Complex Relationship with Thyroid Function
The relationship between caffeine and thyroid function is complex. While moderate caffeine consumption is generally considered safe, excessive intake may interfere with thyroid hormone absorption, especially when consumed close to taking thyroid medication.
Caffeine can also contribute to increased anxiety and sleep disturbances, which are common symptoms of thyroid disorders. How can you manage caffeine consumption with hypothyroidism?
Balancing Caffeine Intake
- Limit caffeine consumption to moderate levels
- Avoid consuming caffeine within an hour of taking thyroid medication
- Be mindful of hidden sources of caffeine, such as chocolate and some medications
- Consider switching to decaffeinated alternatives if sensitive to caffeine
Alcohol: Potential Impacts on Thyroid Health
While moderate alcohol consumption is generally considered safe for most people, those with hypothyroidism should be cautious. Alcohol can interfere with thyroid hormone production and may exacerbate symptoms of hypothyroidism.
Additionally, alcohol can contribute to liver damage, which plays a crucial role in converting T4 to the active T3 hormone. How can you approach alcohol consumption if you have hypothyroidism?
Managing Alcohol Intake
- Limit alcohol consumption to moderate levels, if at all
- Be aware of potential interactions between alcohol and thyroid medication
- Consider non-alcoholic alternatives for social situations
- Consult with your healthcare provider about safe alcohol consumption
Nutrient-Dense Foods for Thyroid Health
While it’s important to know which foods to avoid, focusing on nutrient-dense foods that support thyroid health is equally crucial. A balanced diet rich in essential nutrients can help manage hypothyroidism symptoms and support overall well-being.
Key nutrients for thyroid health include iodine, selenium, zinc, and vitamins A, D, and B12. Which foods are particularly beneficial for those with hypothyroidism?
Thyroid-Friendly Foods
- Fish and seafood (rich in iodine and selenium)
- Brazil nuts (high in selenium)
- Lean meats (good source of zinc)
- Eggs (contain iodine and selenium)
- Fruits and vegetables (rich in antioxidants and vitamins)
- Greek yogurt (high in protein and probiotics)
Incorporating these foods into your diet can help support thyroid function and overall health. Remember to consult with a healthcare provider or registered dietitian for personalized dietary advice.
The Role of Supplements in Managing Hypothyroidism
While a balanced diet should be the primary source of nutrients, some individuals with hypothyroidism may benefit from targeted supplementation. However, it’s crucial to approach supplements cautiously, as some can interfere with thyroid function or medication absorption.
Which supplements are commonly considered for hypothyroidism? How should they be used?
Potential Supplements for Hypothyroidism
- Selenium: May support thyroid hormone production
- Vitamin D: Often deficient in those with thyroid disorders
- Probiotics: Can support gut health and potentially improve thyroid function
- B-complex vitamins: Important for energy production and metabolism
Always consult with a healthcare provider before starting any supplement regimen. They can help determine which supplements, if any, are appropriate for your individual needs and ensure they won’t interfere with your thyroid medication.
Strategies for Long-Term Thyroid Health
Managing hypothyroidism goes beyond just avoiding certain foods. A comprehensive approach to thyroid health involves lifestyle factors, regular medical check-ups, and consistent medication management. What strategies can help maintain long-term thyroid health?
Holistic Approaches to Thyroid Management
- Maintain a consistent sleep schedule to support hormone balance
- Engage in regular physical activity, which can boost metabolism and energy levels
- Manage stress through relaxation techniques like meditation or yoga
- Stay hydrated to support overall metabolic function
- Work with a healthcare team to regularly monitor thyroid function and adjust treatment as needed
Remember, thyroid health is a journey, and what works best may vary from person to person. Be patient with your body and work closely with your healthcare providers to find the most effective management strategies for you.
Navigating Social Situations with Dietary Restrictions
Managing dietary restrictions for hypothyroidism can be challenging, especially in social situations. How can you navigate dining out, parties, and other events while maintaining your thyroid-friendly diet?
Tips for Social Eating with Hypothyroidism
- Inform hosts or restaurants about your dietary needs in advance
- Offer to bring a dish you can eat to gatherings
- Research restaurant menus beforehand to identify suitable options
- Don’t be afraid to ask for modifications to menu items
- Keep thyroid-friendly snacks on hand for unexpected situations
By planning ahead and communicating your needs, you can enjoy social situations while still adhering to your dietary guidelines.
The Future of Thyroid Research and Treatment
As our understanding of thyroid disorders continues to evolve, new research is shedding light on potential treatments and management strategies. What exciting developments are on the horizon for hypothyroidism treatment?
Emerging Areas in Thyroid Research
- Personalized medicine approaches based on genetic profiles
- Investigation of the gut-thyroid axis and the role of the microbiome
- Development of new thyroid hormone analogues
- Exploration of environmental factors influencing thyroid health
- Advanced imaging techniques for more accurate thyroid diagnostics
While these areas of research hold promise, it’s important to continue following current evidence-based guidelines for thyroid management. Stay informed about new developments by discussing them with your healthcare provider.
Managing hypothyroidism through diet and lifestyle choices is an ongoing process. By understanding which foods to avoid, focusing on nutrient-dense options, and working closely with healthcare providers, individuals with hypothyroidism can optimize their thyroid function and overall well-being. Remember, everyone’s journey with thyroid health is unique, and what works best may vary from person to person. Stay informed, be proactive in your health management, and don’t hesitate to seek support when needed.
Various Possible Toxicants Involved in Thyroid Dysfunction: A Review
J Clin Diagn Res. 2016 Jan; 10(1): FE01–FE03.
,1,2 and 3
Jagminder K. Bajaj
1 Professor and Head, Department of Pharmacology, PIMS, Jalandhar, India.
Poonam Salwan
2 Assistant Professor, Department of Pharmacology, SGT Medical College and Hospital, Gurgaon, India.
Shalini Salwan
3 Associate Professor, Department of Pharmacology, PIMS, Jalandhar, India.
1 Professor and Head, Department of Pharmacology, PIMS, Jalandhar, India.
2 Assistant Professor, Department of Pharmacology, SGT Medical College and Hospital, Gurgaon, India.
3 Associate Professor, Department of Pharmacology, PIMS, Jalandhar, India.
Corresponding author.NAME, ADDRESS, E-MAIL ID OF THE CORRESPONDING AUTHOR: Dr. Shalini Salwan, Associate Professor, Department of Pharmacology, PIMS, Jalandhar-144001, India. E-mail: ni.oc.oohay@nawlasinilahsrd
Received 2015 Jun 12; Revisions requested 2015 Aug 28; Accepted 2015 Oct 28.
Copyright © 2016 Journal of Clinical and Diagnostic ResearchThis article has been cited by other articles in PMC.
Abstract
About 300 million people across the world suffer from thyroid gland dysfunction. Environmental factors play an important role in causation of autoimmune thyroid diseases in susceptible individuals. Genetics contributes to 70% of the risk. In order to reduce the risk, we need to understand the association of environmental agents with thyroid dysfunction. These factors are especially relevant for those at increased risk due to positive family history. The ideal study to see the impact of a thyroid toxicant consists of directly measuring the degree of exposure to toxicant in an individual with his thyroid status. Knowledge of various factors influencing thyroid dysfunction can help in interpreting the results of such studies in a better way. This article is an attempt to highlight the various possible toxicants affecting thyroid function so that adequate measures can be undertaken to control excessive exposure in future to reduce the prevalence of thyroid disorders.
Keywords: Goiter, Hypothyroidism, Thyroid disorders, Thyroid
Introduction
Thyroid gland produces three important metabolic hormones, thyroxine, tri-iodothyronine, and calcitonin [1]. Thyroid stimulating hormone (TSH) produced by the anterior pituitary gland controls the production of these hormones. Iodine, derived mainly from sea-foods or consumed in the form of iodized salt, is utilized for producing T3 and T4 hormones [2]. Thyroid Disorders are the commonest amongst the various glandular disorders of the endocrine system [3]. According to a recently released report, about 300 million people in the world are suffering from this endocrine problem, out of which 42 million are Indians [4,5]. The prevalence of thyroid disorders is not distinctive in different age groups, sex as well as different areas [6]. Common thyroid disorders include hypothyroidism, hyperthyroidism, goiter and other Iodine deficiency disorders, Hashimoto’s thyroiditis and thyroid cancer [7]. The untreated thyroid disease can produce serious consequences especially cardiovascular diseases. So, improved public awareness about thyroid disorders and the responsible factors for it is important to cope with thyroid illness [8].
The prevalence of hypothyroidism in 8 major cities of India is reported to be 10.95% with significantly higher proportion of females vs. males (15.86% vs. 5.02%) and older vs. younger (13.11% vs. 7.53%) adults and 21.85% patients tested positive for anti-TPO antibodies [9]. Another study however showed the prevalence of hypothyroidism to be 3.9%; out of which 53% of subjects with subclinical hypothyroidism were positive for anti-TPO antibodies. Urinary iodine status in the same population showed it to be iodine sufficient. Anti-TPO antibodies reported in more than a third of community detected hyperthyroid cases [10]. In the past, endemic goiter has been linked to iodine deficiency by several prominent researchers [11–13] but despite iodization, its prevalence has not reduced, hence thyroid auto-immunity and other goitrogens seem to play important role in causation of goiter [14].
Genetic predisposition is reported in about 70-80% of autoimmune thyroid disease [15], the rest 20-30% contributed by environmental triggers based on animal and human studies [16–19]. Thus, the knowledge of environmental factors that trigger autoimmune thyroid diseasemay help in reducing the risk [20].
Some of the factors proposed from various human and animal studies are:
Dietary Factors
Excess dietary iodine: In genetically susceptible individuals, increased consumption of Iodine can act as a trigger for thyroiditis [21,22]. Iodine laden foods viz. kelp seaweed, iodinated salt, iodine additives to bread /flour, preservatives, medicines such as amiodarone, vitamins, Lugol’sIodine topical antiseptics and contrast dyes may act as starting point as highly iodinated thyroglobulin is demonstrated to be more immunogenic than poorly iodinated one [23–25]. Iodine may also have a direct toxic effect on thyroid via free oxygen radicals and immune stimulation [26].
Naturally occurring goitrogens: They are found in legumes, plants, amiodarone, lithium [27], in addition to cabbage, cauliflower, broccoli, turnip, forms of root cassava. Soy or soy enriched foods can also aggravate thyroid problems reducing T4 absorption and interfering with thyroid hormone action [28] and are reported to increase auto-immune thyroid disease [29].
Role of Dietary Fat: Nutrition can affect hypothalamo-pituitary thyroidal axis [30]. Dietary fat composition influences TSH secretion, thyroid peroxidase activity, hepatic deiodinase activities and T3 binding to nuclear receptors. In a study conducted on male Wistar rats, fed on diets differing in fat composition, total and free thyroxine levels were found to be higher in saturated fat fed group than others. Further Tri-iodothyronine and thyroid peroxidase levels were reported to decrease in rats fed on polyunsaturated fats and increased in rats fed on monounsaturated fats. However, hepatic de iodinase activity decreased irrespective of fat composition [31]. TPO activity might be stimulated by consumption of polyunsaturated n-3 FA and monounsaturated n-9 FA while it is reduced by saturated and polyunsaturated n-6 FA. Stimulating effects of n-3 PUFA have also been observed for transthyretin expression in brain [32] and thyrocyte proliferation [33]. However, other results also suggest involvement of PUFA n-6 in stimulation of thyroid activity [34]. Dietary high–fat lard intake induced significant thyroid dysfunction and abnormal morphology in rats which failed to be corrected by short-term dietary modification. Raised triglyceride levels and decreased total T4 and free T4 levels along with raised serum TSH levels were noted [35]. In another study on rat model, the effect of thermally oxidized dietary fats was noted. Raised plasma thyroxine concentration showed that oxidized fats can also alter the morphology and function of thyroid gland [36].
Role of Green Tea: Thyroid function can be impaired by green tea extracts at high doses. A significant decrease in serum T3 and T4 and increase in TSH levels has been reported along with decreased TPO and deiodinase activity in response to dietary green tea extract in rats [37]. A recent study conducted to see the effect of catechins, the flavonoids in green tea on thyroid physiology in rat model concluded decreased activity of thyroid peroxide and 5’-deiodinaseI enzymes. Decreased levels of serum T3 and T4 along with significant elevation of TSH was noted [38].
Soy and Soybean Ppoduct: One of the studies reported the development of goiter and hypothyroidism in a 10-month-old infant who was put on soybean product right from birth but it reversed with soybean product withdrawal and Lugol’s iodine drops. In addition, thyroid showed high uptake of I131 after soybean product withdrawal. Studies on adults revealed significant suppression in plasma-bound I131 while receiving soybean product [39]. Thus soybean product seemed to contain goitrogenic agent which affects thyroid function. A review of 14 trials concluded that although soya protein and isoflavones do not affect normal thyroid function in people with sufficient iodine intake but they may interfere with absorption of synthetic thyroid hormone increasing the dose of medication in hypothyroid patients [40].
Cyanogenic Plant Foods: Raw, boiled and cooked extracts of various cyanogenic plant foods including cauliflower, cabbage, mustard, turnip, raddish, bamboo shoot and cassava have been shown to possess anti-TPO activity. Moreover, boiled exracts of these cyanogenic plant foods showed highest anti-TPO potency followed by cooked and raw extracts. Goitrin is an active goitrogen present in plants of Rutabaga, turnip and Brassicae seeds. However, cooking destroys the enzyme responsible for activation of progoitrin to goitrin thus negating its anti-thyroidal potency. Goitrogenic foods if consumed in considerable quantities may contribute to development of goiter but it is difficult to incriminate them as aetiologic factors in vast majority of goitrous patients [41].
Role of Groundnut: The effects of groundnut supplements on size and iodine content of thyroid and radioactive I131 uptake and its urinary excretion were studied in albino rats. Groundnuts (active principle arachidoside) were reported to be goitrogenic, however this effect was inhibited by small amounts of iodine as potassium iodide [42,43].
Role of Millet: Various studies on rats and thyroid slices of pork have shown that millet diets containing C-glycosylflavones (glycosylvitexin, glycosylorientin and vitexin) produce effects resembling small doses of anti-thyroid drug, methimazole. Maximum anti-thyroid effect and significant increase in thyroid weight along with maximum inhibition of TPO activity was seen with millet bran fraction having maximum concentration C-glycosylflavones [44].
Selenium deficiency and Vitamin B12 deficiency have also been implicated in autoimmune thyroiditis [45].
Environmental Factors
Organochlorine compounds found in pesticides, induce hepatic enzymes leading to decreased half-life of serum thyroxine (T4) [46].
Isoflavones: reduce thyroperoxidase activity [47].
Polychlorinated biphenyls, polybrominateddiphenylethers, bisphenol-A, and triclosan may have direct action on thyroid hormone receptor [47].
Perchlorates found in rocket fuels, thiocyanates and nitrates interfere with iodine uptake [47]. A study conducted on pregnant women living in an industrial area in south California showed strong association between increased urinary perchlorate and decreased total and free thyroxine levels along with increased TSH levels [48].
Cosmetics: UV filters meant to protect skin from UV irradiation can also alter thyroid homeostasis [49]. A study on Benzophenone-2 treated rats showed low T4 levels and high TSH levels besides altered Thyroid-peroxidase activity [49]. Another chemical OMC (Octyl-methoxycinnamate)causes dose dependent decrease in serum T3 and T4 concentration in rats [50].
Heavy metals: Heavy metals like cadmium and lead are known to affect thyroid function. In a study on adult cows, lead exposed cows living in polluted areas showed significantly higher blood lead and T3, T4 concentration [51]. In a study on pregnant women, those from lead exposed town had lower mean free thyroxine (FT4), higher mean TPO antibodies along with higher lead concentration suggesting stimulation of auto-immunity by prolonged lead exposure [52].
Studies using genetically exposed mice have also shown bromine and bacterial lipopolysaccharides to triggerautoimmune thyroiditis [53].
In the third National Health and Nutrition Examination Survey (NHANESIII), relationship between smoking and thyroid abnormalities was evaluated. Smoking has been found to be inversely related to the prevalence of serum thyroid auto-antibodies. Lesser number of smokers were shown to have serum thyroid auto-antibodies (11%) and elevated TSH (2.6%) in comparison to non-smokers (18%) and (5.5%) respectively [54].
Role of Age: Thyroid diseases are reported to be more common in perimenopausal and menopausal women because of altered balance between oestrogen and progesterone [55], However, daily administration of genisteinaglycone (a known goitrogen) to post-menopausal women over a period of 3 years did not modify T3, T4, TSH levels and enzyme activity [56] hence proving there is no relation of age to thyroid diseases.
Conclusion
The goitrogenic potential of a plant or food depends upon the amount of active goitrogen present in it. Various procedures like soaking, washing, boiling and cooking can help in reducing the goitrogenic potency of these foods. These, along with the intake of iodide supplements are generally practiced in areas where goitrogenic foods are routinely consumed. How far these measures are effective in reducing anti-thyroidal activity is still unclear. Patients suffering from hypothyroidism can avoid consumption of raw cruciferous vegetables such as cabbage, Brussels sprouts, broccoli, cauliflower, mustard greens, kale, and turnip. In addition, daily diet should include thyroid boosting foods like those rich in iodine, amino acid tyrosine, minerals like selenium, zinc, copper, iron, various vitamins including, B2, B3, B6, C and E. The benefits of iodine repletion outweigh the risk of thyroid auto-immunity, hence global iodine sufficiency should be ensured. The amount of fat consumed and its composition definitely influences thyroid activity as evident from the study quoted above but more studies are required to validate the results. It is difficult to prove the role of environmental chemicals in increasing susceptibility to autoimmune thyroid disease although they have been blamed for its causation since long. Further studies on environmental toxicants can provide an indepth view of the impact of these agents.
Notes
Financial or Other Competing Interests
None.
References
[1] Canaris GJ, Manowitz NR, Mayor G, Ridgway EC. The Colorado thyroid disease prevalence study. ArchInt Med. 2000;160:526–34. [PubMed] [Google Scholar][2] Lamfon HA. Thyroid disorders in Makkah. Saudiean J Appl Sci. 2008;1:55–58. [Google Scholar][3] Kochupillai N. Clinical Endocrinology in India. Curr Sci. 2000;79:1061–70. [Google Scholar][6] Larsen PR, Davies TF, Hay ID. Williams Text book of Endocrinology. 9th ed. Philadelphia: Saunders; 1988. TheThyroid. In: Williams Wilson JD, Foster DW, Kronenberg HM, editors; pp. 389–416. [Google Scholar][7] Unnikrishnan AG, Menon UV. Thyroid disorders in India: An epidemiological perspective. Indian J Endocrinol Metab. 2011;15(Suppl2):S78–S81. [PMC free article] [PubMed] [Google Scholar][8] Antony J, Celine TM, Chacko M. Spectrum of thyroid disorders: A retrospective study at a medical college hospital. Thyroid Res Pract. 2014;11:55–59. [Google Scholar][9] Unnikrishnan AG, Kalra S, Sahay RK, Bantwal G, John M, Tewari N. Prevalence of hypothyroidism in adults: An epidemiological study in eight cities of India. Indian J Endocrinol Metab. 2013;17(4):647–52. [PMC free article] [PubMed] [Google Scholar][10] Menon UV, Sundaram KR, Unnikrishnan AG, Jayakumar RV, Nair V, Kumar H. High Prevalence of undetected thyroid disorders in an iodine sufficient adult south Indian population. J Indian Med Assoc. 2009;107:72–77. [PubMed] [Google Scholar][11] Karmarkar MG, Deo MG, Kochupillai N, Ramachandran K, Ramalingaswami V. Pathophysiology of Himalayan endemic goiter. Am J Clin Nutr. 1974;27:96–103. [PubMed] [Google Scholar][12] Sooch SS, Deo MG, Karmarkar MG, Kochupillai N, Ramachandran K, Ramalingaswami V. Prevention of endemic goiter with iodized salt.1973. Natl Med J India. 2001;14:185–88. [PubMed] [Google Scholar][13] Pandav CS, Karmarkar MG, Kochupillai N. Recommended levels of salt iodation in India. Indian J Pediatr. 1984;51:53–54. [PubMed] [Google Scholar][14] Marwaha RK, Tandon N, Gupta N, Karak AK, Verma K, Kochupillai N. Residual Goitre in the postiodizationphase:Iodine status, thiocyanate exposure and autoimmunity. Clin Endocrinol(Oxf) 2003;59:672–81. [PubMed] [Google Scholar][15] Hansen PS, Brix TH, Iachine I, Kyvik KO, Hegedus L. The relevant importance of genetic and environmental effects for early stages of thyroid autoimmunity: a study of healthy Danish twins. Eur J Endocrinol. 2006;154:29–38. [PubMed] [Google Scholar][16] Streider TGA, Tijssen JGP, Wenzel BE, Endert E, Wiersinga WM. Prediction of progression to overt hypothyroidism or hyperthyroidism in female relatives of patients with auto-immune thyroid disease using the thyroid events Amsterdam(THEA) score. Arch Intern Med. 2008;168:1657–63. [PubMed] [Google Scholar][17] Prummel MF, Streider T, Wiersinga WM. The environment and autoimmune thyroid diseases. Eur J Endocrinol. 2004;150:605–18. [PubMed] [Google Scholar][19] Tanda ML, Piantinida E, Lai A, Lombardi V, Dalle Mule I, Liparulo L, et al. Thyroid autoimmunity and environment. Horm Metab Res. 2009;41:436–42. [PubMed] [Google Scholar][21] Tajiri J, Higashi K, Morita M, Umeda T, Sato T. Studies of hypothyroidism in patients with high iodine intake. J Clin Endocrinol Metab. 1986;63:412–17. [PubMed] [Google Scholar][22] Kampe O, Jansson R, Karlsson FA. Effects of L-thyroxine and iodide on the development of autoimmune postpartum thyroiditis. J Clin Endocrinol Metab. 1990;70:1014–18. [PubMed] [Google Scholar][23] Saboori AM, Rose NR, Bresler HS, Vladut-Talor M, Burek CL. Iodination of human thyroglobulin(Tg) alters its immunoreactivity. I. Iodination alters multiple epitopes of human Tg. Clin Exp Immunol. 1998;113:297–302. [PMC free article] [PubMed] [Google Scholar][24] Saboori AM, Rose NR, Burek CL. Iodination of human thyroglobulin (Tg) alters its immunoreactivity. II. Fine specificity of a monoclonal antibody that recognizes iodinated Tg. Clin Exp Immunol. 1998;113:303–08. [PMC free article] [PubMed] [Google Scholar][25] Rasooly L, Rose NR, Saboori AM, Ladenson PW, Burek CL. Iodine is essential for human T cell recognition of human thyroglobulin. Autoimmunity. 1998;27:213–19. [PubMed] [Google Scholar][26] Papanastasiou L, Vatalas IA, Koutras DA, Mastorakas G. Thyroid autoimmunity in the current iodine environment. Thyroid. 2007;17:729–39. [PubMed] [Google Scholar][27] Sharma RB, Burek CL, Cihakova D, Njoku DB, Rose NR. Autoimmune diseases in Endocrinology. Totowa NJ: Humana Press; 2008. Environmental factors in autoimmune endocrinopathies. In: Weetman AP, Editor; pp. 35–75. [Google Scholar][28] Messina M, Redmond G. Effects of soy protein and soybean isoflavones on thyroid functions in healthy adults and thyroid patients: a review of relevant literature. Thyroid. 2006;16:249–58. [PubMed] [Google Scholar][29] Fort P, Moses N, Fasano M, Goldberg T, Lifshitz F. Breast and soy formula feedings in early infancy and the prevalence of autoimmune thyroid disease in children. J Am Coll Nutr. 1990;9:164–67. [PubMed] [Google Scholar][30] Kopp W. Nutrition, evaluation and thyroid hormone levels – a link to iodine deficiency disorders? Med Hypotheses. 2004;62:871–75. [PubMed] [Google Scholar][31] Lachowicz K, Koszela-Piotrowska I, Rosolowska-Huszcz D. Thyroid hormone metabolism may depend on dietary fat. Journal of animal and feed sciences. 2008;17:110–19. [Google Scholar][32] Puskas LG, Kitajka K, Nyakas C, Barcelo-Coblijn G, Farkas T. Short-term adm. of omega-3 FA from fish oil results in increased transthyretin transcription in old rat hippocampus. Proc Nat Acad Sci USA. 2003;100:1580–85. [PMC free article] [PubMed] [Google Scholar][33] Makino M, Oda N, Miura N, Imamura S, Yamamoto K, Kato T, et al. Effect of eicosapentaenoic acid ethyl ester on hypothyroid function. J Endocrinol. 2001;171:259–65. [PubMed] [Google Scholar][34] Forman BM, Tontonoz P, Chen J, Brun RP, Spiegalman BM, Evans RM. 15-deoxy-delta 12,14-prostaglandin J2 is a ligand for the adipocyte determination factor PPAR gamma. Cell. 1995;83:803–12. [PubMed] [Google Scholar][35] Shao SS, Zhao YF, Song YF, Xu C, Yang JM, Xuan SM, et al. Dietary high-fat lard intake induces thyroid dysfunction and abnormal morphology in rats. Acta Pharmacol Sin. 2014;35(11):1411–20. [PMC free article] [PubMed] [Google Scholar][36] Eder K, SKufca P, Brandsch C. Thermally oxidized dietary fats increase plasma thyroxine concentrations in rats irrespective of the vitamin E and selenium supply. J Nutr. 2002;132(6):1275–81. [PubMed] [Google Scholar][37] Chandra AK, De N. Goitrogenic/antithyroidal potential of green tea extract in relation to catechin in rats. Food and chemical Toxicology. 2010;48:2304–11. [PubMed] [Google Scholar][38] Chandra AK, De N. Catechin induced modulation in the activities of thyroid hormone synthesizing enzymes leading to hypothyroidism. Mol Cell Biochem. 2013;374(1-2):37–48. [PubMed] [Google Scholar][39] Van Wyk JJ, Arnold Mary B, Wynn J, Pepper F. The effects of a soybean product on thyroid function in humans. Pediatrics. 1959;24(5):752–60. [PubMed] [Google Scholar][40] Chandra AK, Mukhopadhyay S, Lahari D, Tripathi S. Goitrogenic content of Indian cyanogenic plant foods and their in vitro anti-thyroidal activity. Indian J Med Res. 2004;119:180–85. [PubMed] [Google Scholar][41] Greer MA. Goitrogenic substances in food. Am J Clin Nutr. 1957;5(4):440–44. [PubMed] [Google Scholar][42] Srinivasan V, Moudgal NR, Sarma PS. Studies on goitrogenic agents in food: Goitrogenic action of Groundnut. JN The Journal of Nutrition. 1956:87–95. [PubMed] [Google Scholar][43] Moudgal NR, Srinivasan V, Sarma PS. Studies on goitrogenic agents in food: Goitrogenic action of Arachidoside. JN The Journal of Nutrition. 1956:89–96. [Google Scholar][44] Gaitan E, Lindsay RH, Reichert RD, Ingbar SH, Cooksey RC, Legan J, et al. Anti-thyroid and goitrogenic effects of millet:role of C-glycosylflavones. J Clin Endocrinol Metab. 1989;68(4):707–14. [PubMed] [Google Scholar][45] Duntas LH. Selenium and the thyroid: a close knit connection. J Clin Endocrinol Metab. 2010;95(12):5180–88. [PubMed] [Google Scholar][46] Pearce EN, Braverman LE. Environmental pollutants and the thyroid. Best Pract Res Clin Endocrinol Metab. 2009;23(6):801–13. [PubMed] [Google Scholar][47] Bahn AK, Mills JL, Synder PJ, Gann PH, Houten L, Bialik O, et al. Hypothyroidism in workers exposed to polybrominated biphenyls. NEngl J Med. 1980;302:31–33. [PubMed] [Google Scholar][48] Steinmaus C, Pearl M, Kharrazi M, Blount BC, Miller MD, Pearce EN, et al. Thyroid hormones and Moderate Exposure to Perchlorate during pregnancy in women in South California. Environ Health Perspect. 2015 [PMC free article] [PubMed] [Google Scholar][49] Schmutzler C, Bacinski A, Gotthardt I, Huhne K, Ambrugger P, Klammer H, et al. The Ultraviolet filter benzophenone-2 interferes with the thyroi hormone axis in rats and is a potent in vitro inhibitor of human recombinant thyroid peroxidase. Endocrinology. 2007;148:2835–44. [PubMed] [Google Scholar][50] Klammer H, Schlecht C, Wuttke W, Schmutzler C, Gotthardt I, Kohrle J, et al. Effects of 5-day treatment with UV-filter octyl-methoxycinnamate (OMC) on the function of hypothalamo-pituitary-thyroid function in rats. Toxicology. 2007;238:192–99. [PubMed] [Google Scholar][51] Swarup D, Naresh R, Varshney VP, Balagangatharathilagar M, Kumar P, Nandi D, et al. Changes in plasma hormone profile and liver function in cows naturally exposed to lead and cadmium around different industrial areas. Res Vet Sci. 2007;82:16–21. [PubMed] [Google Scholar][52] Kahn LG, Liu X, Rajovic B, Popovac D, Oberfield S, Joseph H, et al. Blood lead concentration and Thyroid function during pregnancy: Results from yugoslavia Prospective study of environmental lead exposure. Environmental Health Perspect. 2014;122(10):1134–40. [PMC free article] [PubMed] [Google Scholar][54] Belin RM, Astor BC, Powe NR, Ladenson PW. Smoke exposure is associated with a lower prevalence of serum thyroid autoantibodies and thyrotropin conc. Elevation and a higher prevalence of mild thyrotropin conc. Suppression in the third National Health and Nutrition Exam. Survey (NHANES III) J Clin Endocrinol Metab. 2004;89(12):6077–86. [PubMed] [Google Scholar][55] Duncan AM, Underhill KE, Xu X, Lavelleur J, Phipps WR, Kurzer MS. Modest hormonal effects of soy Isoflavones in post-menopausal women. J Clin Endocrinol Metab. 1999;84:3479–84. [PubMed] [Google Scholar][56] Bitto A, Polito F, Atteritano M, Altavilla D, Mazzaferro S, Marini H, et al. Genisteinaglycone does not affect thyroid function: results from a 3-year randomised double blind placebo controlled trial. J Clin Endocrinol Metab. 2010;95:3067–72. [PubMed] [Google Scholar]
Various Possible Toxicants Involved in Thyroid Dysfunction: A Review
J Clin Diagn Res. 2016 Jan; 10(1): FE01–FE03.
,1,2 and 3
Jagminder K. Bajaj
1 Professor and Head, Department of Pharmacology, PIMS, Jalandhar, India.
Poonam Salwan
2 Assistant Professor, Department of Pharmacology, SGT Medical College and Hospital, Gurgaon, India.
Shalini Salwan
3 Associate Professor, Department of Pharmacology, PIMS, Jalandhar, India.
1 Professor and Head, Department of Pharmacology, PIMS, Jalandhar, India.
2 Assistant Professor, Department of Pharmacology, SGT Medical College and Hospital, Gurgaon, India.
3 Associate Professor, Department of Pharmacology, PIMS, Jalandhar, India.
Corresponding author.NAME, ADDRESS, E-MAIL ID OF THE CORRESPONDING AUTHOR: Dr. Shalini Salwan, Associate Professor, Department of Pharmacology, PIMS, Jalandhar-144001, India. E-mail: ni.oc.oohay@nawlasinilahsrd
Received 2015 Jun 12; Revisions requested 2015 Aug 28; Accepted 2015 Oct 28.
Copyright © 2016 Journal of Clinical and Diagnostic ResearchThis article has been cited by other articles in PMC.
Abstract
About 300 million people across the world suffer from thyroid gland dysfunction. Environmental factors play an important role in causation of autoimmune thyroid diseases in susceptible individuals. Genetics contributes to 70% of the risk. In order to reduce the risk, we need to understand the association of environmental agents with thyroid dysfunction. These factors are especially relevant for those at increased risk due to positive family history. The ideal study to see the impact of a thyroid toxicant consists of directly measuring the degree of exposure to toxicant in an individual with his thyroid status. Knowledge of various factors influencing thyroid dysfunction can help in interpreting the results of such studies in a better way. This article is an attempt to highlight the various possible toxicants affecting thyroid function so that adequate measures can be undertaken to control excessive exposure in future to reduce the prevalence of thyroid disorders.
Keywords: Goiter, Hypothyroidism, Thyroid disorders, Thyroid
Introduction
Thyroid gland produces three important metabolic hormones, thyroxine, tri-iodothyronine, and calcitonin [1]. Thyroid stimulating hormone (TSH) produced by the anterior pituitary gland controls the production of these hormones. Iodine, derived mainly from sea-foods or consumed in the form of iodized salt, is utilized for producing T3 and T4 hormones [2]. Thyroid Disorders are the commonest amongst the various glandular disorders of the endocrine system [3]. According to a recently released report, about 300 million people in the world are suffering from this endocrine problem, out of which 42 million are Indians [4,5]. The prevalence of thyroid disorders is not distinctive in different age groups, sex as well as different areas [6]. Common thyroid disorders include hypothyroidism, hyperthyroidism, goiter and other Iodine deficiency disorders, Hashimoto’s thyroiditis and thyroid cancer [7]. The untreated thyroid disease can produce serious consequences especially cardiovascular diseases. So, improved public awareness about thyroid disorders and the responsible factors for it is important to cope with thyroid illness [8].
The prevalence of hypothyroidism in 8 major cities of India is reported to be 10.95% with significantly higher proportion of females vs. males (15.86% vs. 5.02%) and older vs. younger (13.11% vs. 7.53%) adults and 21.85% patients tested positive for anti-TPO antibodies [9]. Another study however showed the prevalence of hypothyroidism to be 3.9%; out of which 53% of subjects with subclinical hypothyroidism were positive for anti-TPO antibodies. Urinary iodine status in the same population showed it to be iodine sufficient. Anti-TPO antibodies reported in more than a third of community detected hyperthyroid cases [10]. In the past, endemic goiter has been linked to iodine deficiency by several prominent researchers [11–13] but despite iodization, its prevalence has not reduced, hence thyroid auto-immunity and other goitrogens seem to play important role in causation of goiter [14].
Genetic predisposition is reported in about 70-80% of autoimmune thyroid disease [15], the rest 20-30% contributed by environmental triggers based on animal and human studies [16–19]. Thus, the knowledge of environmental factors that trigger autoimmune thyroid diseasemay help in reducing the risk [20].
Some of the factors proposed from various human and animal studies are:
Dietary Factors
Excess dietary iodine: In genetically susceptible individuals, increased consumption of Iodine can act as a trigger for thyroiditis [21,22]. Iodine laden foods viz. kelp seaweed, iodinated salt, iodine additives to bread /flour, preservatives, medicines such as amiodarone, vitamins, Lugol’sIodine topical antiseptics and contrast dyes may act as starting point as highly iodinated thyroglobulin is demonstrated to be more immunogenic than poorly iodinated one [23–25]. Iodine may also have a direct toxic effect on thyroid via free oxygen radicals and immune stimulation [26].
Naturally occurring goitrogens: They are found in legumes, plants, amiodarone, lithium [27], in addition to cabbage, cauliflower, broccoli, turnip, forms of root cassava. Soy or soy enriched foods can also aggravate thyroid problems reducing T4 absorption and interfering with thyroid hormone action [28] and are reported to increase auto-immune thyroid disease [29].
Role of Dietary Fat: Nutrition can affect hypothalamo-pituitary thyroidal axis [30]. Dietary fat composition influences TSH secretion, thyroid peroxidase activity, hepatic deiodinase activities and T3 binding to nuclear receptors. In a study conducted on male Wistar rats, fed on diets differing in fat composition, total and free thyroxine levels were found to be higher in saturated fat fed group than others. Further Tri-iodothyronine and thyroid peroxidase levels were reported to decrease in rats fed on polyunsaturated fats and increased in rats fed on monounsaturated fats. However, hepatic de iodinase activity decreased irrespective of fat composition [31]. TPO activity might be stimulated by consumption of polyunsaturated n-3 FA and monounsaturated n-9 FA while it is reduced by saturated and polyunsaturated n-6 FA. Stimulating effects of n-3 PUFA have also been observed for transthyretin expression in brain [32] and thyrocyte proliferation [33]. However, other results also suggest involvement of PUFA n-6 in stimulation of thyroid activity [34]. Dietary high–fat lard intake induced significant thyroid dysfunction and abnormal morphology in rats which failed to be corrected by short-term dietary modification. Raised triglyceride levels and decreased total T4 and free T4 levels along with raised serum TSH levels were noted [35]. In another study on rat model, the effect of thermally oxidized dietary fats was noted. Raised plasma thyroxine concentration showed that oxidized fats can also alter the morphology and function of thyroid gland [36].
Role of Green Tea: Thyroid function can be impaired by green tea extracts at high doses. A significant decrease in serum T3 and T4 and increase in TSH levels has been reported along with decreased TPO and deiodinase activity in response to dietary green tea extract in rats [37]. A recent study conducted to see the effect of catechins, the flavonoids in green tea on thyroid physiology in rat model concluded decreased activity of thyroid peroxide and 5’-deiodinaseI enzymes. Decreased levels of serum T3 and T4 along with significant elevation of TSH was noted [38].
Soy and Soybean Ppoduct: One of the studies reported the development of goiter and hypothyroidism in a 10-month-old infant who was put on soybean product right from birth but it reversed with soybean product withdrawal and Lugol’s iodine drops. In addition, thyroid showed high uptake of I131 after soybean product withdrawal. Studies on adults revealed significant suppression in plasma-bound I131 while receiving soybean product [39]. Thus soybean product seemed to contain goitrogenic agent which affects thyroid function. A review of 14 trials concluded that although soya protein and isoflavones do not affect normal thyroid function in people with sufficient iodine intake but they may interfere with absorption of synthetic thyroid hormone increasing the dose of medication in hypothyroid patients [40].
Cyanogenic Plant Foods: Raw, boiled and cooked extracts of various cyanogenic plant foods including cauliflower, cabbage, mustard, turnip, raddish, bamboo shoot and cassava have been shown to possess anti-TPO activity. Moreover, boiled exracts of these cyanogenic plant foods showed highest anti-TPO potency followed by cooked and raw extracts. Goitrin is an active goitrogen present in plants of Rutabaga, turnip and Brassicae seeds. However, cooking destroys the enzyme responsible for activation of progoitrin to goitrin thus negating its anti-thyroidal potency. Goitrogenic foods if consumed in considerable quantities may contribute to development of goiter but it is difficult to incriminate them as aetiologic factors in vast majority of goitrous patients [41].
Role of Groundnut: The effects of groundnut supplements on size and iodine content of thyroid and radioactive I131 uptake and its urinary excretion were studied in albino rats. Groundnuts (active principle arachidoside) were reported to be goitrogenic, however this effect was inhibited by small amounts of iodine as potassium iodide [42,43].
Role of Millet: Various studies on rats and thyroid slices of pork have shown that millet diets containing C-glycosylflavones (glycosylvitexin, glycosylorientin and vitexin) produce effects resembling small doses of anti-thyroid drug, methimazole. Maximum anti-thyroid effect and significant increase in thyroid weight along with maximum inhibition of TPO activity was seen with millet bran fraction having maximum concentration C-glycosylflavones [44].
Selenium deficiency and Vitamin B12 deficiency have also been implicated in autoimmune thyroiditis [45].
Environmental Factors
Organochlorine compounds found in pesticides, induce hepatic enzymes leading to decreased half-life of serum thyroxine (T4) [46].
Isoflavones: reduce thyroperoxidase activity [47].
Polychlorinated biphenyls, polybrominateddiphenylethers, bisphenol-A, and triclosan may have direct action on thyroid hormone receptor [47].
Perchlorates found in rocket fuels, thiocyanates and nitrates interfere with iodine uptake [47]. A study conducted on pregnant women living in an industrial area in south California showed strong association between increased urinary perchlorate and decreased total and free thyroxine levels along with increased TSH levels [48].
Cosmetics: UV filters meant to protect skin from UV irradiation can also alter thyroid homeostasis [49]. A study on Benzophenone-2 treated rats showed low T4 levels and high TSH levels besides altered Thyroid-peroxidase activity [49]. Another chemical OMC (Octyl-methoxycinnamate)causes dose dependent decrease in serum T3 and T4 concentration in rats [50].
Heavy metals: Heavy metals like cadmium and lead are known to affect thyroid function. In a study on adult cows, lead exposed cows living in polluted areas showed significantly higher blood lead and T3, T4 concentration [51]. In a study on pregnant women, those from lead exposed town had lower mean free thyroxine (FT4), higher mean TPO antibodies along with higher lead concentration suggesting stimulation of auto-immunity by prolonged lead exposure [52].
Studies using genetically exposed mice have also shown bromine and bacterial lipopolysaccharides to triggerautoimmune thyroiditis [53].
In the third National Health and Nutrition Examination Survey (NHANESIII), relationship between smoking and thyroid abnormalities was evaluated. Smoking has been found to be inversely related to the prevalence of serum thyroid auto-antibodies. Lesser number of smokers were shown to have serum thyroid auto-antibodies (11%) and elevated TSH (2.6%) in comparison to non-smokers (18%) and (5.5%) respectively [54].
Role of Age: Thyroid diseases are reported to be more common in perimenopausal and menopausal women because of altered balance between oestrogen and progesterone [55], However, daily administration of genisteinaglycone (a known goitrogen) to post-menopausal women over a period of 3 years did not modify T3, T4, TSH levels and enzyme activity [56] hence proving there is no relation of age to thyroid diseases.
Conclusion
The goitrogenic potential of a plant or food depends upon the amount of active goitrogen present in it. Various procedures like soaking, washing, boiling and cooking can help in reducing the goitrogenic potency of these foods. These, along with the intake of iodide supplements are generally practiced in areas where goitrogenic foods are routinely consumed. How far these measures are effective in reducing anti-thyroidal activity is still unclear. Patients suffering from hypothyroidism can avoid consumption of raw cruciferous vegetables such as cabbage, Brussels sprouts, broccoli, cauliflower, mustard greens, kale, and turnip. In addition, daily diet should include thyroid boosting foods like those rich in iodine, amino acid tyrosine, minerals like selenium, zinc, copper, iron, various vitamins including, B2, B3, B6, C and E. The benefits of iodine repletion outweigh the risk of thyroid auto-immunity, hence global iodine sufficiency should be ensured. The amount of fat consumed and its composition definitely influences thyroid activity as evident from the study quoted above but more studies are required to validate the results. It is difficult to prove the role of environmental chemicals in increasing susceptibility to autoimmune thyroid disease although they have been blamed for its causation since long. Further studies on environmental toxicants can provide an indepth view of the impact of these agents.
Notes
Financial or Other Competing Interests
None.
References
[1] Canaris GJ, Manowitz NR, Mayor G, Ridgway EC. The Colorado thyroid disease prevalence study. ArchInt Med. 2000;160:526–34. [PubMed] [Google Scholar][2] Lamfon HA. Thyroid disorders in Makkah. Saudiean J Appl Sci. 2008;1:55–58. [Google Scholar][3] Kochupillai N. Clinical Endocrinology in India. Curr Sci. 2000;79:1061–70. [Google Scholar][6] Larsen PR, Davies TF, Hay ID. Williams Text book of Endocrinology. 9th ed. Philadelphia: Saunders; 1988. TheThyroid. In: Williams Wilson JD, Foster DW, Kronenberg HM, editors; pp. 389–416. [Google Scholar][7] Unnikrishnan AG, Menon UV. Thyroid disorders in India: An epidemiological perspective. Indian J Endocrinol Metab. 2011;15(Suppl2):S78–S81. [PMC free article] [PubMed] [Google Scholar][8] Antony J, Celine TM, Chacko M. Spectrum of thyroid disorders: A retrospective study at a medical college hospital. Thyroid Res Pract. 2014;11:55–59. [Google Scholar][9] Unnikrishnan AG, Kalra S, Sahay RK, Bantwal G, John M, Tewari N. Prevalence of hypothyroidism in adults: An epidemiological study in eight cities of India. Indian J Endocrinol Metab. 2013;17(4):647–52. [PMC free article] [PubMed] [Google Scholar][10] Menon UV, Sundaram KR, Unnikrishnan AG, Jayakumar RV, Nair V, Kumar H. High Prevalence of undetected thyroid disorders in an iodine sufficient adult south Indian population. J Indian Med Assoc. 2009;107:72–77. [PubMed] [Google Scholar][11] Karmarkar MG, Deo MG, Kochupillai N, Ramachandran K, Ramalingaswami V. Pathophysiology of Himalayan endemic goiter. Am J Clin Nutr. 1974;27:96–103. [PubMed] [Google Scholar][12] Sooch SS, Deo MG, Karmarkar MG, Kochupillai N, Ramachandran K, Ramalingaswami V. Prevention of endemic goiter with iodized salt.1973. Natl Med J India. 2001;14:185–88. [PubMed] [Google Scholar][13] Pandav CS, Karmarkar MG, Kochupillai N. Recommended levels of salt iodation in India. Indian J Pediatr. 1984;51:53–54. [PubMed] [Google Scholar][14] Marwaha RK, Tandon N, Gupta N, Karak AK, Verma K, Kochupillai N. Residual Goitre in the postiodizationphase:Iodine status, thiocyanate exposure and autoimmunity. Clin Endocrinol(Oxf) 2003;59:672–81. [PubMed] [Google Scholar][15] Hansen PS, Brix TH, Iachine I, Kyvik KO, Hegedus L. The relevant importance of genetic and environmental effects for early stages of thyroid autoimmunity: a study of healthy Danish twins. Eur J Endocrinol. 2006;154:29–38. [PubMed] [Google Scholar][16] Streider TGA, Tijssen JGP, Wenzel BE, Endert E, Wiersinga WM. Prediction of progression to overt hypothyroidism or hyperthyroidism in female relatives of patients with auto-immune thyroid disease using the thyroid events Amsterdam(THEA) score. Arch Intern Med. 2008;168:1657–63. [PubMed] [Google Scholar][17] Prummel MF, Streider T, Wiersinga WM. The environment and autoimmune thyroid diseases. Eur J Endocrinol. 2004;150:605–18. [PubMed] [Google Scholar][19] Tanda ML, Piantinida E, Lai A, Lombardi V, Dalle Mule I, Liparulo L, et al. Thyroid autoimmunity and environment. Horm Metab Res. 2009;41:436–42. [PubMed] [Google Scholar][21] Tajiri J, Higashi K, Morita M, Umeda T, Sato T. Studies of hypothyroidism in patients with high iodine intake. J Clin Endocrinol Metab. 1986;63:412–17. [PubMed] [Google Scholar][22] Kampe O, Jansson R, Karlsson FA. Effects of L-thyroxine and iodide on the development of autoimmune postpartum thyroiditis. J Clin Endocrinol Metab. 1990;70:1014–18. [PubMed] [Google Scholar][23] Saboori AM, Rose NR, Bresler HS, Vladut-Talor M, Burek CL. Iodination of human thyroglobulin(Tg) alters its immunoreactivity. I. Iodination alters multiple epitopes of human Tg. Clin Exp Immunol. 1998;113:297–302. [PMC free article] [PubMed] [Google Scholar][24] Saboori AM, Rose NR, Burek CL. Iodination of human thyroglobulin (Tg) alters its immunoreactivity. II. Fine specificity of a monoclonal antibody that recognizes iodinated Tg. Clin Exp Immunol. 1998;113:303–08. [PMC free article] [PubMed] [Google Scholar][25] Rasooly L, Rose NR, Saboori AM, Ladenson PW, Burek CL. Iodine is essential for human T cell recognition of human thyroglobulin. Autoimmunity. 1998;27:213–19. [PubMed] [Google Scholar][26] Papanastasiou L, Vatalas IA, Koutras DA, Mastorakas G. Thyroid autoimmunity in the current iodine environment. Thyroid. 2007;17:729–39. [PubMed] [Google Scholar][27] Sharma RB, Burek CL, Cihakova D, Njoku DB, Rose NR. Autoimmune diseases in Endocrinology. Totowa NJ: Humana Press; 2008. Environmental factors in autoimmune endocrinopathies. In: Weetman AP, Editor; pp. 35–75. [Google Scholar][28] Messina M, Redmond G. Effects of soy protein and soybean isoflavones on thyroid functions in healthy adults and thyroid patients: a review of relevant literature. Thyroid. 2006;16:249–58. [PubMed] [Google Scholar][29] Fort P, Moses N, Fasano M, Goldberg T, Lifshitz F. Breast and soy formula feedings in early infancy and the prevalence of autoimmune thyroid disease in children. J Am Coll Nutr. 1990;9:164–67. [PubMed] [Google Scholar][30] Kopp W. Nutrition, evaluation and thyroid hormone levels – a link to iodine deficiency disorders? Med Hypotheses. 2004;62:871–75. [PubMed] [Google Scholar][31] Lachowicz K, Koszela-Piotrowska I, Rosolowska-Huszcz D. Thyroid hormone metabolism may depend on dietary fat. Journal of animal and feed sciences. 2008;17:110–19. [Google Scholar][32] Puskas LG, Kitajka K, Nyakas C, Barcelo-Coblijn G, Farkas T. Short-term adm. of omega-3 FA from fish oil results in increased transthyretin transcription in old rat hippocampus. Proc Nat Acad Sci USA. 2003;100:1580–85. [PMC free article] [PubMed] [Google Scholar][33] Makino M, Oda N, Miura N, Imamura S, Yamamoto K, Kato T, et al. Effect of eicosapentaenoic acid ethyl ester on hypothyroid function. J Endocrinol. 2001;171:259–65. [PubMed] [Google Scholar][34] Forman BM, Tontonoz P, Chen J, Brun RP, Spiegalman BM, Evans RM. 15-deoxy-delta 12,14-prostaglandin J2 is a ligand for the adipocyte determination factor PPAR gamma. Cell. 1995;83:803–12. [PubMed] [Google Scholar][35] Shao SS, Zhao YF, Song YF, Xu C, Yang JM, Xuan SM, et al. Dietary high-fat lard intake induces thyroid dysfunction and abnormal morphology in rats. Acta Pharmacol Sin. 2014;35(11):1411–20. [PMC free article] [PubMed] [Google Scholar][36] Eder K, SKufca P, Brandsch C. Thermally oxidized dietary fats increase plasma thyroxine concentrations in rats irrespective of the vitamin E and selenium supply. J Nutr. 2002;132(6):1275–81. [PubMed] [Google Scholar][37] Chandra AK, De N. Goitrogenic/antithyroidal potential of green tea extract in relation to catechin in rats. Food and chemical Toxicology. 2010;48:2304–11. [PubMed] [Google Scholar][38] Chandra AK, De N. Catechin induced modulation in the activities of thyroid hormone synthesizing enzymes leading to hypothyroidism. Mol Cell Biochem. 2013;374(1-2):37–48. [PubMed] [Google Scholar][39] Van Wyk JJ, Arnold Mary B, Wynn J, Pepper F. The effects of a soybean product on thyroid function in humans. Pediatrics. 1959;24(5):752–60. [PubMed] [Google Scholar][40] Chandra AK, Mukhopadhyay S, Lahari D, Tripathi S. Goitrogenic content of Indian cyanogenic plant foods and their in vitro anti-thyroidal activity. Indian J Med Res. 2004;119:180–85. [PubMed] [Google Scholar][41] Greer MA. Goitrogenic substances in food. Am J Clin Nutr. 1957;5(4):440–44. [PubMed] [Google Scholar][42] Srinivasan V, Moudgal NR, Sarma PS. Studies on goitrogenic agents in food: Goitrogenic action of Groundnut. JN The Journal of Nutrition. 1956:87–95. [PubMed] [Google Scholar][43] Moudgal NR, Srinivasan V, Sarma PS. Studies on goitrogenic agents in food: Goitrogenic action of Arachidoside. JN The Journal of Nutrition. 1956:89–96. [Google Scholar][44] Gaitan E, Lindsay RH, Reichert RD, Ingbar SH, Cooksey RC, Legan J, et al. Anti-thyroid and goitrogenic effects of millet:role of C-glycosylflavones. J Clin Endocrinol Metab. 1989;68(4):707–14. [PubMed] [Google Scholar][45] Duntas LH. Selenium and the thyroid: a close knit connection. J Clin Endocrinol Metab. 2010;95(12):5180–88. [PubMed] [Google Scholar][46] Pearce EN, Braverman LE. Environmental pollutants and the thyroid. Best Pract Res Clin Endocrinol Metab. 2009;23(6):801–13. [PubMed] [Google Scholar][47] Bahn AK, Mills JL, Synder PJ, Gann PH, Houten L, Bialik O, et al. Hypothyroidism in workers exposed to polybrominated biphenyls. NEngl J Med. 1980;302:31–33. [PubMed] [Google Scholar][48] Steinmaus C, Pearl M, Kharrazi M, Blount BC, Miller MD, Pearce EN, et al. Thyroid hormones and Moderate Exposure to Perchlorate during pregnancy in women in South California. Environ Health Perspect. 2015 [PMC free article] [PubMed] [Google Scholar][49] Schmutzler C, Bacinski A, Gotthardt I, Huhne K, Ambrugger P, Klammer H, et al. The Ultraviolet filter benzophenone-2 interferes with the thyroi hormone axis in rats and is a potent in vitro inhibitor of human recombinant thyroid peroxidase. Endocrinology. 2007;148:2835–44. [PubMed] [Google Scholar][50] Klammer H, Schlecht C, Wuttke W, Schmutzler C, Gotthardt I, Kohrle J, et al. Effects of 5-day treatment with UV-filter octyl-methoxycinnamate (OMC) on the function of hypothalamo-pituitary-thyroid function in rats. Toxicology. 2007;238:192–99. [PubMed] [Google Scholar][51] Swarup D, Naresh R, Varshney VP, Balagangatharathilagar M, Kumar P, Nandi D, et al. Changes in plasma hormone profile and liver function in cows naturally exposed to lead and cadmium around different industrial areas. Res Vet Sci. 2007;82:16–21. [PubMed] [Google Scholar][52] Kahn LG, Liu X, Rajovic B, Popovac D, Oberfield S, Joseph H, et al. Blood lead concentration and Thyroid function during pregnancy: Results from yugoslavia Prospective study of environmental lead exposure. Environmental Health Perspect. 2014;122(10):1134–40. [PMC free article] [PubMed] [Google Scholar][54] Belin RM, Astor BC, Powe NR, Ladenson PW. Smoke exposure is associated with a lower prevalence of serum thyroid autoantibodies and thyrotropin conc. Elevation and a higher prevalence of mild thyrotropin conc. Suppression in the third National Health and Nutrition Exam. Survey (NHANES III) J Clin Endocrinol Metab. 2004;89(12):6077–86. [PubMed] [Google Scholar][55] Duncan AM, Underhill KE, Xu X, Lavelleur J, Phipps WR, Kurzer MS. Modest hormonal effects of soy Isoflavones in post-menopausal women. J Clin Endocrinol Metab. 1999;84:3479–84. [PubMed] [Google Scholar][56] Bitto A, Polito F, Atteritano M, Altavilla D, Mazzaferro S, Marini H, et al. Genisteinaglycone does not affect thyroid function: results from a 3-year randomised double blind placebo controlled trial. J Clin Endocrinol Metab. 2010;95:3067–72. [PubMed] [Google Scholar]
a countrywide case-control study in New Caledonia
Cancer Causes Control. Author manuscript; available in PMC 2012 Nov 13.
Published in final edited form as:
PMCID: PMC3496161
HALMS: HALMS471339
INSERM Subrepository
Thérèse Truong
1CESP, Centre de recherche en épidémiologie et santé des populations
INSERM : U1018, Université Paris XI – Paris Sud, Hôpital Paul Brousse, Assistance publique – Hôpitaux de Paris (AP-HP), 16 avenue Paul Vaillant Couturier 94807 Villejuif Cedex, France,FR
Dominique Baron-Dubourdieu
2Laboratory of Anatomy and Cytopathology
Nouméa,NC
Yannick Rougier
3Institut Pasteur de Nouvelle-Calédonie
Réseau International des Instituts Pasteur, B.P. 61 98845 Nouméa,NC
Pascal Guénel
1CESP, Centre de recherche en épidémiologie et santé des populations
INSERM : U1018, Université Paris XI – Paris Sud, Hôpital Paul Brousse, Assistance publique – Hôpitaux de Paris (AP-HP), 16 avenue Paul Vaillant Couturier 94807 Villejuif Cedex, France,FR
1CESP, Centre de recherche en épidémiologie et santé des populations
INSERM : U1018, Université Paris XI – Paris Sud, Hôpital Paul Brousse, Assistance publique – Hôpitaux de Paris (AP-HP), 16 avenue Paul Vaillant Couturier 94807 Villejuif Cedex, France,FR
2Laboratory of Anatomy and Cytopathology
Nouméa,NC
3Institut Pasteur de Nouvelle-Calédonie
Réseau International des Instituts Pasteur, B.P. 61 98845 Nouméa,NC
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Abstract
Exceptionally high incidence rates of thyroid cancer have been reported in New Caledonia, particularly in Melanesian women. To clarify the reasons of this elevated incidence, we conducted a countrywide population-based case-control study in the multiethnic population of Caledonian women. The study included 293 cases of thyroid cancer and 354 population controls. Based on a food frequency questionnaire, we investigated the role in thyroid cancer of food items rich in iodine – such as seafood – and of vegetables containing goitrogens – such as cruciferous vegetables. A measure of total daily iodine intake based on a food composition table was also used. Our findings provided little support for an association between thyroid cancer and consumption of fish and seafood. We found that high consumption of cruciferous vegetables was associated with thyroid cancer among women with low iodine intake (OR=1.86; 95% CI: 1.01–3.43 for iodine intake < 96 μg/day). The high consumption of cruciferous vegetables among Melanesian women, a group with mild iodine deficiency, may contribute to explain the exceptionally high incidence of thyroid cancer in this group.
Keywords: Adult, Aged, Aged, 80 and over, Brassica, Case-Control Studies, Diet, Female, Humans, Iodine, administration & dosage, Male, Middle Aged, New Caledonia, epidemiology, Questionnaires, Thyroid Neoplasms, epidemiology, etiology, Vegetables, Young Adult
Keywords: case-control study, diet, iodine, New caledonia, thyroid neoplasms
The incidence of thyroid cancer is elevated in South Pacific, particularly in New Caledonia (1), a French overseas territory of approximately 200,000 inhabitants including native Melanesians (44%), Europeans (34%) and other ethnic groups (22%) of Polynesian or Asian origin (2). In a previous paper, we reported very high annual incidence rates for all ethnic groups in the period 1985–1999, particularly in Melanesian women (71.4/100,000) and men (10.4/100,000) (1). As in other countries around the world, a sharp increase in incidence was observed in New Caledonia after the introduction of improved techniques of thyroid cancer screening in 1995, but the background incidence of thyroid cancer has been exceptionally elevated in this population since at least 1985 (3). Exposure to ionizing radiations during childhood is the only well-established risk factor for thyroid cancer. Unlike French Polynesia, it should be pointed out that no nuclear test was conducted in New Caledonia, making unclear the causes of this elevated incidence. In order to identify new risk factors for thyroid cancer, we conducted a countrywide population-based case-control study of thyroid cancer in New Caledonia. In previous papers (4, 5) we reported that high parity and obesity may be partly responsible for the high incidence among Melanesian women. In the present paper, we examine the role of dietary factors that interfere with thyroid function, such as food with high iodine concentration and vegetables containing goitrogenic substances.
Rat experiments have shown that both iodine-rich and iodine-deficient diet induce thyroid follicular tumorigenesis, possibly through promoting effects of thyreostimulin (TSH) (6;7). It has been suggested that the increased incidence of thyroid papillary carcinoma observed in many countries during the last decades may be related to the introduction of iodine prophylaxis, mainly through salt iodization. However, the increasing incidence could also be attributed to the improvement of screening procedures that have led to enhanced detection of occult papillary carcinomas during the same period (1;8;9). Only two epidemiological studies have investigated the role of iodine intake in thyroid cancer, and reported a positive association in Hawaii (10) and an inverse association in the San Francisco Bay area (11).
Cruciferous vegetables contain thioglucosides that are metabolized to thiocyanates. These compounds inhibit iodine transport and the incorporation of iodide into thyroglobulin, thus increasing TSH secretion and thyroid cells proliferation. In animal experiments, it has been found that these substances induce thyroid carcinomas (12). Another group of potent goitrogens are contained in food such as cassava or sweet potatoes, with high content of cyanogenic glycosides (13). In epidemiological studies, no clear association between thyroid cancer and cruciferous vegetables or other food items containing goitrogens has been demonstrated (14, 10, 15).
In the present study, we focused on food items known to be rich in iodine such as fish, seafood, milk and dairy products and on total dietary intake of iodine. We also studied the role of cruciferous vegetables, starchy food and cassava containing goitrogenic substances. A possible interaction between iodine deficiency and high consumption of cruciferous vegetables was examined, as both variables decrease the iodine absorption by the thyroid gland and may enhance thyroid stimulation by the TSH. All the analyses were restricted to women, since the group of men was too small for meaningful analyses.
MATERIAL AND METHODS
Case selection
The cases eligible to the study were patients with papillary or follicular thyroid carcinoma diagnosed between January 1, 1993, and December 31, 1999, who had been living in New Caledonia for at least 5 years at the time of cancer diagnosis.
The cases were identified from the pathology records of the two histopathology laboratories of New Caledonia, one public and one private. The ascertainment of cases was completed by searches in medical records of the main hospitals, and in the Cancer Registry of New Caledonia that also records cancer diagnoses from medical facilities throughout the country. All the pathology reports, and if not sufficient, the original histological slides, were reviewed in order to confirm the histological diagnosis and to determine the number and size of the cancerous nodules.
Cases were recruited at the beginning of the data collection in 1998, retrospectively for those diagnosed between 1993 and 1997, and prospectively for those diagnosed in 1998 and 1999. The good prognosis of papillary and follicular thyroid cancer enabled to contact most cases several years after diagnosis. Of 324 eligible cases of thyroid cancer in women, 31 could not be interviewed because the subject had died (n=18), refused to participate (n=8), could not be contacted (n=4) or was too ill to answer (n=1). Finally, 293 cases of thyroid cancer in women (response rate 90 percent) were included in the study, of whom 255 were papillary and 38 were follicular carcinomas.
Control selection
Controls were selected from electoral rolls recently updated at the time of study initiation in 1998 that included all New Caledonia residents aged 18 years or older. Seven groups of controls were constituted, each corresponding to a group of cases with a given year of diagnosis of the study period (1993–1999). Each control group was formed from a random selection of women in the electoral rolls in order to frequency-match the corresponding group of cases by 5-year age group. Controls were allocated a year of reference equal to the year of diagnosis of the case group for which they were selected. To be eligible a control should have been living in New Caledonia for at least 5 years at the year of reference and should not have had a thyroid cancer before that date.
Of 405 eligible control women, 51 were not interviewed because they were dead at the time of the interview (n=11), refused to participate (n=19), could not be contacted (n=18), were too ill to answer (n=2) or for another reason (n=1). Finally, 354 controls in women (response rate 87 percent) were included in the analysis.
Data collection
In-person interviews were conducted by trained interviewers at the subject’s home using a structured questionnaire. We collected data on sociodemographic characteristics, diet, alcohol consumption, tobacco smoking, anthropometric factors, hormonal and reproductive factors, previous medical conditions, medical x-ray exposure, residential history, and family history of cancer or benign thyroid conditions. Only exposures or events which occurred before the year of diagnosis for the cases or the year of reference for the controls were taken into account.
We used a food-frequency questionnaire including 110 items to assess the dietary habits during the previous 5-year period. The frequency of fruits and vegetables consumption was corrected to take the seasonality into account. Portion size was determined using color photographs representing each item in 3 commonly eaten amounts. Information on seasonality and weight of local fruits and vegetables were determined with a local nutritionist. The daily consumption of a food item was then estimated in grams. The 110 food items were grouped into 25 food groups. In the present paper, the following food groups were analyzed: salt water fish, brackish water fish, seafood, dairy products, cruciferous vegetables, and starchy foods.
Total energy intake (kilo-calories/day) was estimated using food composition tables developed for France (16) and for the Pacific Islands (17). Iodine intake was computed using a French food composition table (18), which includes information on iodine content for most food items in France, but not for some local New Caledonia seafood such as giant clam, coconut crab, mangrove crab, and freshwater prawn. These food items were omitted because their consumption was negligible as compared to more common fishes and seafood.
Statistical analysis
The odds ratios (OR) and their 95 percent confidence intervals (CI) were calculated by unconditional logistic regression, using SAS version 9. Food items consumptions were divided into tertiles on the basis of the distribution among controls for each ethnic group. Odds ratios were adjusted for age (5-year age groups), energy intake and ethnic group. Because the dietary profile depended on the ethnic origin, analyses were also conducted separately for the two main ethnic groups (European, Melanesian). All analyses conducted separately among Melanesian women were adjusted for the Province of residence (North, South, Loyalty Islands). Food items consumption and iodine intake were categorized into tertiles on the basis of the distribution among controls. If more than 33 percent of the controls declared that they never consumed a given food item, we used non-consumers as the reference category, and we divided consumers into two classes using the median of the distribution among controls. Tests for trend were calculated by fitting a model where the median value of each class was used as a quantitative variable. Multivariate models were used to take into account potential confounding from risk factors associated with thyroid cancer risk in our data (ever had a miscarriage, irregular menstruations, number of full-term pregnancies, body mass index) (4;5). As the results were unchanged, odds ratios adjusted for these variables are not shown.
RESULTS
The socio-demographic characteristics of the cases and the controls are shown in . Because of the frequency-matched design of the study, the distribution by age was similar in the two groups (chi-square test: P=0.66). Proportionally more cases than controls were of Melanesian origin, and among Melanesian women more cases than controls were living in the Loyalty Islands. No statistically significant difference between cases and controls was observed with respect to educational level after adjustment for age and ethnicity.
Table 1
Sociodemographic Characteristics of Thyroid Cancer Cases and Controls – New Caledonia, 1993–1999.
Cases (n=293) | Controls (n=354) | OR | 95% CI | |||
---|---|---|---|---|---|---|
n | % | n | % | |||
Age (years) | ||||||
<25 | 10 | 3.4 | 13 | 3.7 | ||
25–29 | 24 | 8.2 | 24 | 6.8 | ||
30–34 | 34 | 11.6 | 42 | 11.9 | ||
35–39 | 32 | 10.9 | 38 | 10.7 | ||
40–44 | 29 | 9.9 | 37 | 10.5 | ||
45–49 | 36 | 12.3 | 32 | 9.0 | ||
50–54 | 30 | 10.2 | 41 | 11.6 | ||
55–59 | 40 | 13.7 | 37 | 10.5 | ||
60–64 | 24 | 8.2 | 44 | 12.4 | ||
65–69 | 18 | 6.1 | 19 | 5.4 | ||
≥70 | 16 | 5.5 | 27 | 7.6 | ||
Ethnic groupa | ||||||
Melanesian | 220 | 75.1 | 169 | 47.7 | 4.30 | 2.74, 6.75 |
European | 32 | 10.9 | 110 | 31.1 | 1.00 | Referent |
Other | 41 | 14.0 | 75 | 21.2 | 1.70 | 0.97, 2.98 |
Province (Melanesians only)a | ||||||
South | 69 | 31.4 | 70 | 41.4 | 1.00 | Referent |
North | 60 | 27.3 | 47 | 27.8 | 1.33 | 0.83, 2.49 |
Loyalty Islands | 91 | 41.4 | 52 | 30.8 | 1.91 | 1.15, 3.15 |
Years of educationb | ||||||
Never went to school | 22 | 7.5 | 20 | 5.7 | 1.10 | 0.55, 2.22 |
≤5 years | 151 | 51.5 | 177 | 50.0 | 1.00 | Referent |
6–9 years | 74 | 25.3 | 94 | 26.6 | 1.12 | 0.72, 1.76 |
≥10 years | 22 | 7.5 | 44 | 12.4 | 1.22 | 0.62, 2.39 |
Missing | 24 | 8.2 | 19 | 5.4 | 1.63 | 0.82, 3.21 |
shows the mean values of body mass index, daily energy intake, iodine intake and intake of selected food groups among control women, according to ethnicity and Province for Melanesian women. The mean dietary intakes differed markedly between European women and Melanesian women, particularly those from the Northern Province and the Loyalty Islands. The dietary profile of Melanesian women from the Southern Province was intermediate between that of European women (most of them living in the South) and Melanesian women in other areas. Other ethnic group women generally had food intakes close to that of the European women. As an example of specific dietary habits, it can be pointed out that brackish water fish was almost exclusively consumed by Melanesian women from the North. Milk and dairy products were consumed in greater amounts by European and other ethnic group women than by Melanesians. The Melanesian women in the Northern Province and in the Loyalty Islands had higher consumptions of cruciferous vegetables and starchy food and lower iodine intake than the other groups of women. The types of cruciferous vegetables also differed between ethnic groups.
Table 2
BMI, total energy intake, and mean daily intake of selected food items among control women by ethnic group and by Province of residence – New Caledonia, 1993–1999
Daily intakeb | Melanesian | European | Other | p-valuea | ||
---|---|---|---|---|---|---|
South | North | Loyalty Islands | n=110 | n=75 | ||
n=70 | n=47 | n=52 | ||||
BMI (kg/m2) | 26.7 | 26.9 | 27.4 | 24.5 | 25.8 | p=0.01 |
Total energy intake (kcal) | 1995.1 | 2397.3 | 2036.4 | 1954.7 | 2207.8 | p=0.04 |
Salt water fish (g) | 20.5 | 24.8 | 19.7 | 16.1 | 22.0 | p=0.08 |
Brackish water fish (g) | 2.8 | 9.1 | 0.4 | 0.4 | 0.5 | p<0.01 |
Canned fish (g) | 12.4 | 26.2 | 17.9 | 5.3 | 5.3 | p<0.01 |
Seafood (g) | 12.3 | 9.9 | 5.5 | 9.6 | 6.5 | p=0.29 |
Milk (g) | 120.1 | 44.8 | 50.3 | 150.1 | 152.9 | p=0.01 |
Dairy products (g) | 57.2 | 23.7 | 29.7 | 127.3 | 89.8 | p<0.01 |
Dietary iodine (μg) | 102.9 | 90.4 | 80.7 | 111.3 | 111.1 | p<0.01 |
Non cruciferous vegetables | 152.7 | 150.3 | 209.5 | 209.9 | 170.1 | p=0.01 |
Cruciferous vegetables (g)c | 53.8 | 62.2 | 83.3 | 56.5 | 51.7 | p=0.02 |
Cabbage | 5.6 | 2.8 | 5.8 | 7.1 | 9.3 | p=0.04 |
Chinese cabbage | 23.7 | 20.8 | 28.1 | 16.6 | 16.0 | p=0.03 |
Melanesian cabbage | 10.1 | 20.5 | 32.7 | 1.2 | 0.9 | p<0.01 |
Starchy foods (g)d | 75.2 | 240.7 | 136.5 | 40.4 | 72.8 | p<0.01 |
Cassava | 20.0 | 54.0 | 16.0 | 2.7 | 6.9 | p<0.01 |
presents the odds ratios for food items rich in iodine (fish, seafood, dairy products) or in goitrogenic compounds (cruciferous vegetables, starchy food). No food item rich in iodine was noticeably associated with thyroid cancer, with the exception of brackish water fish that was inversely related to the disease in Melanesian women (p-trend=0.01). The odds ratios for total iodine intake in the second and third tertiles were slightly above unity in Melanesian women, but were below one in European women. For cruciferous vegetables, the odds ratio in the highest tertile among Melanesian women was 1.62 at the limit of statistical significance and the test for trend was 0.09. Again in European women, the odds ratio for cruciferous vegetables was below unity. Consumption of starchy food was slightly associated with thyroid cancer among Europeans only.
Table 3
Odds ratios for thyroid cancer associated with selected food items among women, by ethnic group – New Caledonia, 1993–1999.
All ethnic groups | European | Melanesian | |||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Quantity (g/day) | Ca (293) | Co (354) | ORa | 95% CI | Quantity (g/day) | Ca (32) | Co (110) | ORb | 95% CI | Quantity (g/day) | Ca (215) | Co (165) | ORc | 95% CI | |
Salt water fish | <14.3 | 79 | 111 | 1.00 | Referent | ≤10.0 | 11 | 41 | 1.00 | Referent | <22.5 | 53 | 53 | 1.00 | Referent |
14.3–32.3 | 82 | 118 | 0.79 | 0.51, 1.22 | 10.0–25.9 | 5 | 31 | 0.57 | 0.17, 1.90 | 22.5–39.2 | 63 | 57 | 0.82 | 0.49, 1.36 | |
≥32.3 | 127 | 117 | 0.95 | 0.62, 1.46 | >25.9 | 16 | 38 | 1.26 | 0.49, 3.23 | ≥39.2 | 79 | 55 | 1.07 | 0.64, 1.78 | |
p-trend=0.15 | p-trend=0.78 | p-trend=0.12 | |||||||||||||
Brackish water fish | 0.0 | 254 | 304 | 1.00 | Referent | 0.0 | 30 | 105 | 0.0 | 185 | 129 | 1.00 | Referent | ||
>0.0–10.0 | 27 | 30 | 0.81 | 0.46, 1.44 | >0.0–2.3 | 1 | 4 | >0.0–11.2 | 25 | 20 | 0.87 | 0.42, 1.79 | |||
>10.0 | 12 | 20 | 0.43 | 0.20, 0.93 | >2.3 | 1 | 1 | >11.2 | 10 | 20 | 0.32 | 0.14, 0.77 | |||
p-trend=0.03 | p-trend=0.01 | ||||||||||||||
Seafood | ≤1.5 | 90 | 116 | 1.00 | Referent | ≤2.6 | 9 | 44 | 1.00 | Referent | ≤1.3 | 69 | 57 | 1.00 | Referent |
1.5–7.9 | 109 | 124 | 1.20 | 0.80, 1.79 | 2.6–7.9 | 12 | 31 | 1.95 | 0.70, 5.42 | 1.3–7.2 | 71 | 56 | 0.97 | 0.57, 1.63 | |
>7.9 | 94 | 114 | 1.02 | 0.67, 1.56 | >7.9 | 11 | 35 | 1.24 | 0.43, 3.57 | >7.2 | 80 | 56 | 1.23 | 0.72, 2.10 | |
p-trend=0.37 | p-trend=0.86 | p-trend=0.47 | |||||||||||||
Dairy products tot | ≤40.6 | 121 | 116 | 1.00 | Referent | ≤98.1 | 9 | 37 | 1.00 | Referent | ≤17.6 | 84 | 55 | 1.00 | Referent |
40.6–194.9 | 86 | 117 | 0.95 | 0.62, 1.45 | 98.1–405.0 | 14 | 36 | 1.35 | 0.48, 3.79 | 17.6–91.5 | 60 | 56 | 0.69 | 0.41, 1.16 | |
>194.9 | 86 | 121 | 1.03 | 0.67, 1.59 | >405.0 | 9 | 37 | 0.73 | 0.23, 2.27 | >91.5 | 76 | 58 | 1.00 | 0.59, 1.70 | |
p-trend=0.85 | p-trend=0.32 | p-trend=0.19 | |||||||||||||
Iodine intake (μg/day) | <75.0 | 106 | 117 | 1.00 | Referent | <79.8 | 11 | 36 | 1.00 | Referent | <68.1 | 70 | 55 | 1.00 | Referent |
75.0–112.6 | 83 | 117 | 1.15 | 0.73, 1.80 | 79.8–114.0 | 5 | 36 | 0.26 | 0.06, 1.07 | 68.1–107.1 | 70 | 56 | 1.13 | 0.63, 2.00 | |
≥112.6 | 104 | 120 | 1.13 | 0.68, 1.87 | ≥114.0 | 16 | 38 | 0.53 | 0.14, 1.97 | ≥107.1 | 80 | 58 | 1.38 | 0.71, 2.68 | |
p-trend=0.43 | p-trend=0.95 | p-trend=0.30 | |||||||||||||
Cruciferous vegetables | ≤27.8 | 74 | 116 | 1.00 | Referent | ≤25.7 | 15 | 37 | 1.00 | Referent | ≤28.6 | 54 | 56 | 1.00 | Referent |
27.8–65.4 | 98 | 118 | 1.11 | 0.73, 1.69 | 25.7–66.8 | 7 | 36 | 0.49 | 0.16, 1.47 | 28.6–66.4 | 72 | 56 | 1.23 | 0.72, 2.10 | |
>65.4 | 121 | 120 | 1.39 | 0.91, 2.11 | >66.8 | 10 | 37 | 0.46 | 0.16, 1.37 | >66.4 | 94 | 57 | 1.62 | 0.94, 2.80 | |
p-trend=0.11 | p-trend=0.22 | p-trend=0.09 | |||||||||||||
Starchy food | ≤8.8 | 51 | 114 | 1.00 | Referent | 0.0 | 13 | 56 | 1.00 | Referent | ≤50.4 | 73 | 56 | 1.00 | Referent |
8.8–74.7 | 109 | 118 | 1.22 | 0.76, 1.97 | >0.0–14.8 | 4 | 27 | 0.68 | 0.19, 2.37 | 50.4–133.3 | 77 | 58 | 0.92 | 0.54, 1.57 | |
>74.7 | 133 | 121 | 1.05 | 0.62, 1.78 | >14.8 | 15 | 27 | 2.27 | 0.84, 6.13 | >133.3 | 70 | 54 | 0.84 | 0.44, 1.61 | |
p-trend=0.74 | p-trend=0.05 | p-trend=0.60 | |||||||||||||
Cassava | 0.0 | 98 | 177 | 1.00 | Referent | 0.0 | 20 | 88 | 1.00 | Referent | ≤6.6 | 64 | 51 | 1.00 | Referent |
0.0–14.3 | 86 | 86 | 1.23 | 0.81, 1.89 | >0.0–6.6 | 6 | 15 | 1.97 | 0.61, 6.34 | 6.6–28.6 | 69 | 48 | 0.86 | 0.52, 1.42 | |
>14.3 | 107 | 89 | 1.24 | 0.80, 1.91 | >6.6 | 6 | 7 | 2.52 | 0.65, 9.75 | >28.6 | 85 | 68 | 1.18 | 0.67, 2.07 | |
p-trend=0.50 | p-trend=0.12 | p-trend=0.55 |
In , we defined two groups of women with low or high daily intake of iodine, using the median of the total daily iodine intake among controls as a cut-point (96 μg/day). The mean intake was estimated to be 62 and 143 μg iodine/day in the group below and above the median, respectively. Means in both groups were below the recommended daily iodine intake and correspond to moderate (30–74 μg/day) and mild iodine deficiency (75–149 μg/day) according to WHO criteria (19). The consumption of cruciferous vegetables was associated with a significantly elevated odds ratio in women with low iodine intake (OR=1.86, 95 percent CI: 1.01, 3.43; p-trend 0.06) but not in women with higher iodine intake (interaction p=0.33). No modification effect was apparent for starchy food.
Table 4
Odds ratios for thyroid cancer associated with cruciferous vegetables and starchy food by iodine intake (below or above median) among women – New Caledonia, 1993–1999.
Iodine Intake | |||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|
<96.0 μg/day | ≥96.0 μg/day | Interaction | |||||||||
Ca (149) | Co (175) | OR | 95% CI | Ca (144) | Co (179) | OR | 95% CI | test | |||
Cruciferous vegetables | |||||||||||
≤27.8 | 38 | 67 | 1.00 | Referent | 36 | 49 | 1.00 | Referent | |||
27.8–65.4 | 58 | 63 | 1.47 | 0.82, 2.61 | 40 | 55 | 0.77 | 0.41, 1.46 | |||
>65.4 | 53 | 45 | 1.86 | 1.01, 3.43 | 68 | 75 | 0.98 | 0.55, 1.77 | |||
p-trend=0.06 | p-trend=0.76 | p=0.33 | |||||||||
Starchy foods | |||||||||||
≤8.8 | 25 | 57 | 1.00 | Referent | 26 | 57 | 1.00 | Referent | |||
8.8–74.7 | 70 | 65 | 1.49 | 0.77, 2.89 | 39 | 53 | 1.01 | 0.50, 2.05 | |||
>74.7 | 54 | 52 | 1.07 | 0.50, 2.3 | 79 | 69 | 1.07 | 0.51, 2.26 | |||
p-trend=0.76 | p-trend=0.26 | p=0.86 |
DISCUSSION
We made the hypothesis that the very high incidence of thyroid cancer in New Caledonia was related to candidate risk factors such as iodine and goitrogens, and that the differences in thyroid cancer incidence across ethnic groups and geographic areas within the country could be explained by differences in dietary profiles. Although we included all incident cases that occurred in New Caledonia over a 6-year period, our study is based on a small population and had a limited statistical power, which precluded more detailed analyses by ethnic group and Province of residence. We did not find a consistent pattern of association between food items and thyroid cancer across population subgroups, but interesting clues emerged from the data.
An important strength of the study is the population-based design with exhaustive identification of thyroid cancer cases over the study period, and response rates close to 90 percent among eligible cases and controls. Unlike most previous studies on dietary factors in thyroid cancer, we used an extensive food frequency questionnaire with 110 foods items. We also used a food composition table of iodine content to estimate the daily intake of dietary iodine.
This method has several limitations. Recall bias may occur if study subjects report a different diet depending on their disease status, particularly if the cases are aware of a possible link between a risk factor and the disease. However, at the time of the study, no dietary recommendation program aiming at preventing thyroid diseases in New Caledonia had been conducted by the public health authorities, and the role of diet could not be suggested by the interviewers who were not aware of specific study hypotheses. It is thus very unlikely that the consumption of specific food items was reported differently by cases and controls.
It should also be pointed out that the cases of thyroid cancer were asked to report their dietary habits at the time of diagnosis, although they could be recruited up to 5 years after diagnosis. Reporting dietary habits with a lag of several years may be less accurate than reporting current diet. To avoid differential misclassification between cases and controls, we used a frequency-matched design where controls were attributed a year of reference similar to the year of diagnosis for the cases, and were asked about their dietary habits using the same lag.
Another limitation of this study is the probable difference in iodine contents between food items consumed in metropolitan France, as reported in the food composition table, and food items actually consumed in New Caledonia. As some seafood from New Caledonia are not found in France, it is possible that our measure of daily iodine intake was slightly underestimated. In addition, the consumption of iodized salt could not be evaluated in our study. Alternative methods for measuring iodine intake include the 24-h measurement of urinary iodine, which is impractical in epidemiological studies. Neutron activation analysis has also been used in one study to measure iodine content in toenail clippings (20), but this technique provides an integrated measure of iodine exposure over a 2–4-week period approximately 1 year prior to clipping. The iodine exposure estimate based on the food frequency questionnaire used in our study constituted an alternative to laboratory measurements. Although imprecise and entailing non differential exposure misclassification, it was deemed adequate for estimating the average daily iodine intake over the past few years. The estimate of mean daily intake in our study subjects was 100 μg iodine, a value corresponding to mild iodine deficiency. This result is consistent with a survey carried out in a sample of tribes and communes in New Caledonia based on iodine measurements in urinary samples (unpublished data: http://www.wpro.who.int/NR/rdonlyres/FAF55745-689B-4CAE-87B6-BDCE7950BC3F/0/nec.pdf).
Fish and seafood
We found that the consumption of saltwater fish, canned fish and seafood was not related to thyroid cancer risk. Brackish water fish, almost exclusively consumed by Melanesians from mainland New Caledonia (Northern and Southern provinces) was inversely related to the disease. A pooled analysis of 13 case-control studies conducted in Europe, USA and Asia, reported no overall association of thyroid cancer with fish and shellfish consumption, but results were conflicting across populations (21). Additional studies alternatively reported positive associations with fish sauce, dried or salted fish (11) or processed fish products (22) and negative associations with saltwater fish (23) or fresh fish (22). These inconsistencies between studies may be explained by differences in local iodine availability, and the assumption that high consumption of fish or seafood is protective in areas with severe iodine deficiency, deleterious in areas where iodine is readily available, and has no effect in areas where iodine intake is adequate. This hypothesis is supported in the pooled analysis (21) by the observation of a slight negative association of fish intake with thyroid cancer in areas where iodine deficiency is or was common. The absence of an association between fish and seafood consumption and thyroid cancer in New Caledonia also fits this hypothesis, as only mild iodine deficiency is observed in this country.
Dairy products
The presence of iodine in milk and dairy products is mainly due to the iodophor sanitizing solutions used in the dairy industry. In New Caledonia, no association with dairy products was detected. One study conducted in Norway and Sweden (24) reported an increased risk of thyroid cancer in endemic goiter areas related to high intake of dairy products. It should be noted that the consumption of dairy products was low in New Caledonia as the highest tertile was >195g/day in comparison with the Nordic study where the lowest tertile was <180g/day.
Daily iodine intake
Our data do not provide strong evidence that dietary iodine intake is related to thyroid cancer, although it was negatively but not statistically significantly associated with the disease in European women. In other case-control studies that assessed daily iodine intake from the diet, the Hawaii study (10) reported an elevation in risk (OR=1.6; 95 percent CI: 0.8–3.2) and the San Francisco Bay area study (11) reported an inverse association (OR=0.49; 95 percent CI: 0.29, 0.84) in the highest exposure categories. In the later study, no association with biomarkers of iodine exposure from nail clipping was observed. Both studies were conducted in a multiethnic population with wide variations of iodine intake. Very high levels of iodine intake, i.e. two to three times the recommended daily allowance of 150 μg/day (19), were measured in these studies as compared to the mean intake of 100 μg/day in New Caledonia. The inconsistencies between studies suggest that interactions between dietary and other population-specific risk factors related to lifestyle or environment may exist.
Goitrogenic food groups
There was some indication of a positive association between consumption of cruciferous vegetables and thyroid cancer in Melanesian women. This association was negative, but not statistically significant, in European women. The mean consumption of cruciferous vegetables in Melanesian women was about 70 g/day, a relatively high value in comparison with the average cruciferous vegetable intake of 25–30 g/day in North America, 15–30 g/day in Europe and 40–80 g/day in Asia (25). The consumption of cruciferous vegetables was thus a possible candidate for explaining the elevated incidence of thyroid cancer in this ethnic group. The stronger association of cruciferous vegetables with thyroid cancer (OR=1.86, 95% CI: 1.01, 3.43) in women with daily iodine intake below 96 μg/day, i.e. with moderate iodine deficiency, is of particular interest. This finding is consistent with biological mechanisms indicating that goitrogenic substances contained in cruciferous vegetables inhibits iodine absorption by the thyroid, thus increasing iodine deficiency within the thyroid gland, and thyroid cell growth through TSH stimulation (13). In the pooled analysis of 11 case-controls studies (14), cruciferous vegetables were not associated with thyroid cancer, and no difference between iodine-rich or iodine-deficient areas was apparent. However, among Japanese subjects with more frequent consumption of cruciferous vegetables, an elevated odds ratio was reported (14). High consumption of cruciferous vegetables was associated with increased risk in persons who ever lived in areas of endemic goiters in Sweden (24). An additional study conducted in Kuwait (22), reported an increased risk of thyroid cancer in frequent consumers of cabbage or cauliflower. Conversely, US studies from Los Angeles and Hawaii reported a decreasing risk with frequent intake of turnips and rutabagas (p-trend=0.01) (23) and a negative association with high consumption of cruciferous vegetables (10). As noted previously, these studies were conducted in populations where very high iodine intakes were observed. To our knowledge, no study has previously investigated the role of cruciferous vegetables in persons with low iodine intake assessed at an individual level, as we did in New Caledonia. This result has strong possible biological grounds, and should be confirmed in larger studies.
Thyroid cancer was weakly associated with starchy food in Europeans. Because Europeans had very low consumption of starchy food, this association could be due to chance or possibly to another food item associated with starchy food consumption in this subgroup. We also studied the role of cassava, known to have goitrogenic properties (26;27), but no association with thyroid cancer emerged. To our knowledge, no previous epidemiological study has examined the role of cassava consumption in thyroid cancer.
Our results did not support the hypothesis that the consumption of fish and seafood is related to thyroid cancer, but suggest a positive association between the consumption of cruciferous vegetables and thyroid cancer. In addition, the possible interaction between consumption of cruciferous vegetables and low intake of dietary iodine may constitute an important finding in our study that should be further scrutinized. Since the consumption of cruciferous vegetables is higher and the iodine deficiency is possibly stronger in Melanesian women than in other ethnic groups, these dietary factors may contribute, along with other anthropometric or reproductive risk factors previously identified in this study, to explain the exceptionally high incidence of thyroid cancer in this group.
Acknowledgments
Fundings
This study was supported by grants from the “Fondation de France”, the “Association pour la Recherche contre le Cancer”, and the “Agence Française de Sécurité Sanitaire de l’Environnement et du Travail (AFSSET)”.
The authors wish to thank Dr Jean-Paul Grangeon (Direction des Affaires Sanitaires et Sociales Nouvelle-Calédonie) as well as the Provincial Health Authorities (DPASS Sud, DPASS Nord, DPASS Îles) for their support during data collection. They are particularly grateful to Michèle Reynier who coordinated the interviews of study subjects across New Caledonia. They also thank Dr Pierre Valeix for the iodine content data and Alexandra Suprayen for her help in quantifying local food portion size.
Abbreviations
CI | confidence intervals |
OR | odds ratio |
TSH | thyroid stimulating hormone |
Reference List
1. Truong T, Rougier Y, Dubourdieu D, et al. Time trends and geographic variations for thyroid cancer in New Caledonia, a very high incidence area (1985–1999) Eur J Cancer Prev. 2007;16(1):62–70. [PubMed] [Google Scholar]2. ITSEE-INSEE. Recensement de la population de Nouvelle-Calédonie, principaux tableaux 1996. Nouméa: ITSEE-INSEE; 1997. [Google Scholar]3. Ballivet S, Salmi LR, Dubourdieu D, Bach F. Incidence of thyroid cancer in New Caledonia, South Pacific, during 1985–1992. Am J Epidemiol. 1995;141(8):741–746. [PubMed] [Google Scholar]4. Truong T, Orsi L, Dubourdieu D, Rougier Y, Hemon D, Guenel P. Role of goiter and of menstrual and reproductive factors in thyroid cancer: a population-based case-control study in New Caledonia (South Pacific), a very high incidence area. Am J Epidemiol. 2005;161(11):1056–1065. [PMC free article] [PubMed] [Google Scholar]5. Guignard R, Truong T, Rougier Y, Baron-Dubourdieu D, Guenel P. Alcohol drinking, tobacco smoking, and anthropometric characteristics as risk factors for thyroid cancer: a countrywide case-control study in New Caledonia. Am J Epidemiol. 2007;166(10):1140–1149. [PMC free article] [PubMed] [Google Scholar]6. Kanno J, Onodera H, Furuta K, Maekawa A, Kasuga T, Hayashi Y. Tumor-promoting effects of both iodine deficiency and iodine excess in the rat thyroid. Toxicol Pathol. 1992;20(2):226–235. [PubMed] [Google Scholar]7. Yamashita H, Noguchi S, Murakami N, et al. Effects of dietary iodine on chemical induction of thyroid carcinoma. Acta Pathol Jpn. 1990;40(10):705–712. [PubMed] [Google Scholar]8. Davies L, Welch HG. Increasing Incidence of Thyroid Cancer in the United States, 1973–2002. JAMA: The Journal of the American Medical Association. 2006;295(18):2164–2167. [PubMed] [Google Scholar]9. Verkooijen HM, Fioretta G, Pache JC, et al. Diagnostic changes as a reason for the increase in papillary thyroid cancer incidence in Geneva, Switzerland. Cancer Causes Control. 2003;14(1):13–17. [PubMed] [Google Scholar]10. Kolonel LN, Hankin JH, Wilkens LR, Fukunaga FH, Hinds MW. An epidemiologic study of thyroid cancer in Hawaii. Cancer Causes Control. 1990;1:223–234. [PubMed] [Google Scholar]11. Horn-Ross PL, Morris JS, Lee M, et al. Iodine and thyroid cancer risk among women in a multiethnic population: the Bay Area Thyroid Cancer Study. Cancer Epidemiol Biomarkers Prev. 2001;10(9):979–985. [PubMed] [Google Scholar]12. Kanno J, Matsuoka C, Furuta K, et al. Tumor promoting effect of goitrogens on the rat thyroid. Toxicol Pathol. 1990;18(2):239–246. [PubMed] [Google Scholar]13. Gaitan E. Goitrogens. Baillieres Clin Endocrinol Metab. 1988;2(3):683–702. [PubMed] [Google Scholar]14. Bosetti C, Negri E, Kolonel L, et al. A pooled analysis of case-control studies of thyroid cancer. VII. Cruciferous and other vegetables (International) Cancer Causes Control. 2002;13(8):765–775. [PubMed] [Google Scholar]15. Memon A, Darif M, Al Saleh K, Suresh A. Epidemiology of reproductive and hormonal factors in thyroid cancer: evidence from a case-control study in the Middle East. Int J Cancer. 2002;97(1):82–89. [PubMed] [Google Scholar]16. Favier JC, Ireland-Ripert J, Toque C, Feinberg M. Table de composition. 2 1995. Répertoire général des aliments. [Google Scholar]17. Dignan C, Burlingame B, Kumar S, Aalbersberg W. The Pacific Islands food composition tables. 2 2004. [Google Scholar]18. Table de composition des aliments CIQUAL. Agence Française de Sécurité Sanitaire des Aliments. 2008. [Google Scholar]19. WHO. A guide for programme managers. Geneva, Switzerland: World Health Organization; 2001. Assessment of iodine deficiency disorders and monitoring their elimination. [Google Scholar]20. Horn-Ross PL, John EM, Lee M, et al. Phytoestrogen consumption and breast cancer risk in a multiethnic population: the Bay Area Breast Cancer Study. American Journal of Epidemiology. 2001;154(5):434–441. [PubMed] [Google Scholar]21. Bosetti C, Kolonel L, Negri E, et al. A pooled analysis of case-control studies of thyroid cancer. VI. Fish and shellfish consumption. Cancer Causes Control. 2001;12(4):375–382. [PubMed] [Google Scholar]22. Memon A, Varghese A, Suresh A. Benign thyroid disease and dietary factors in thyroid cancer: a case-control study in Kuwait. Br J Cancer. 2002;86(11):1745–1750. [PMC free article] [PubMed] [Google Scholar]23. Mack WJ, Preston-Martin S, Bernstein L, Qian D. Lifestyle and other risk factors for thyroid cancer in Los Angeles County females. Ann Epidemiol. 2002;12(6):395–401. [PubMed] [Google Scholar]24. Galanti MR, Hansson L, Bergstrom R, et al. Diet and the risk of papillary and follicular thyroid carcinoma: a population-based case-control study in Sweden and Norway. Cancer Causes Control. 1997;8(2):205–214. [PubMed] [Google Scholar]25. IARC. Cruciferous vegetables, isothiocyanates and indoles. Lyon: International Agency for Research on Cancer; 2004. [Google Scholar]26. Ekpechi OL, Dimitriadou A, Fraser R. Goitrogenic activity of cassava (a staple Nigerian food) Nature. 1966;210(5041):1137–1138. [PubMed] [Google Scholar]27. Ermans AM, Delange F, Van d V, Kinthaert J. Goitrogenic action of cyanogenic glucosides present in cassava: a possible etiologic factor of endemic goiter in the Idjwi island. Acta Endocrinol Suppl (Copenh) 1973;179:31. [PubMed] [Google Scholar]
How Raw Cabbage Affects Your Thyroid
Fresh cabbage growing in a garden.
Image Credit: YuriyS/iStock/Getty Images
Your thyroid is a butterfly-shaped gland that sits near your vocal cords and produces the T3 and T4 hormones that control your metabolism. To make these hormones, your body uses iodine — about 80 percent of the iodine you consume is used by your thyroid. If your diet is deficient in iodine, or you have an underactive thyroid, known as hypothyroidism, eating raw cruciferous vegetables such as cabbage can further suppress your thyroid hormone function.
Thyroid Function
Your thyroid produces two distinct hormones, T3 and T4, which regulate the rate your body uses energy and oxygen, which are the two components of your metabolism. If your thyroid doesn’t produce enough hormones, your metabolism slows, leading to weight gain, slower heart rate and an increased sensitivity to cold. The most common cause of hypothyroidism is an autoimmune disorder, but an iodine deficiency can also slow thyroid hormone production. Iodine deficiencies are rare in the United States because salt is iodized specifically to prevent hypothyroidism.
Cruciferous Vegetables
A goiter is an enlarged thyroid gland that indicates hypothyroidism. A goitrogenic food contains a substance that can affect your thyroid, slowing hormone production. Cruciferous vegetables all contain goitrogens. These include all types of cabbages, such as napa cabbage, bok choy and Brussels sprouts; broccoli, cauliflower and kale; and collard, mustard and turnip greens. If you have normal thyroid function and consume adequate amounts of iodine, these compounds will have no effect on your thyroid. The Institute of Medicine has established the recommended dietary allowance, or RDA, for iodine at 150 mcg daily. One tsp. of table salt contains 400 mcg of iodine.
Goitrogens
Fortunately, the goitrogenic compounds in cruciferous vegetables are destroyed by heat. Cooking these vegetables will ensure that they will not affect your thyroid. There are different types of goitrogens; the ones in raw cabbage and other cruciferous vegetables are isothiocyanates, which block the enzyme that allows your thyroid to use iodine. Other foods that contain goitrogens are soy, spinach, strawberries, peaches and peanuts. Fermenting soy disables the goitrogenic isoflavones found in soy foods. Also, you can limit your consumption of certain foods to avoid the goitrogenic effect.
Iodine Deficiency
In developing nations, iodine deficiency is the leading cause of hypothyroidism. In the 1920s, iodine was added to salt in the United States to prevent thyroid problems. If you’re following a low-sodium diet, other food sources of iodine include saltwater fish, shellfish, seaweed, eggs, cheese, ice cream, yogurt, milk, bread and soy sauce. You can also take a daily multivitamin to ensure proper iodine intake. Both too little and too much iodine can create thyroid problems. In rare cases, an increased iodine intake can lead to hyperthyroidism — an overactive thyroid.
Cruciferous Vegetables | Linus Pauling Institute
1. Ishida M, Hara M, Fukino N, Kakizaki T, Morimitsu Y. Glucosinolate metabolism, functionality and breeding for the improvement of Brassicaceae vegetables. Breed Sci. 2014;64(1):48-59. (PubMed)
2. International Agency for Research on Cancer. Cruciferous vegetables. Cruciferous vegetables, isothiocyanates and indoles. Lyon, France: IARC; 2004:1-12.
3. Agerbirk N, Olsen CE. Glucosinolate structures in evolution. Phytochemistry. 2012;77:16-45. (PubMed)
4. Steinbrecher A, Linseisen J. Dietary intake of individual glucosinolates in participants of the EPIC-Heidelberg cohort study. Ann Nutr Metab. 2009;54(2):87-96. (PubMed)
5. Barba FJ, Nikmaram N, Roohinejad S, Khelfa A, Zhu Z, Koubaa M. Bioavailability of glucosinolates and their breakdown products: impact of processing. Front Nutr. 2016;3:24. (PubMed)
6. Luang-In V, Albaser AA, Nueno-Palop C, Bennett MH, Narbad A, Rossiter JT. Glucosinolate and desulfo-glucosinolate metabolism by a selection of human gut bacteria. Curr Microbiol. 2016;73(3):442-451. (PubMed)
7. Fahey JW, Wehage SL, Holtzclaw WD, et al. Protection of humans by plant glucosinolates: efficiency of conversion of glucosinolates to isothiocyanates by the gastrointestinal microflora. Cancer Prev Res (Phila). 2012;5(4):603-611. (PubMed)
8. Verkerk R, Schreiner M, Krumbein A, et al. Glucosinolates in Brassica vegetables: the influence of the food supply chain on intake, bioavailability and human health. Mol Nutr Food Res. 2009;53 Suppl 2:S219. (PubMed)
9. Li F, Hullar MA, Beresford SA, Lampe JW. Variation of glucoraphanin metabolism in vivo and ex vivo by human gut bacteria. Br J Nutr. 2011;106(3):408-416. (PubMed)
10. Liu RH. Potential synergy of phytochemicals in cancer prevention: mechanism of action. J Nutr. 2004;134(12 Suppl):3479S-3485S. (PubMed)
11. McNaughton SA, Marks GC. Development of a food composition database for the estimation of dietary intakes of glucosinolates, the biologically active constituents of cruciferous vegetables. Br J Nutr. 2003;90(3):687-697. (PubMed)
12. Bai Y, Wang X, Zhao S, Ma C, Cui J, Zheng Y. Sulforaphane protects against cardiovascular disease via Nrf2 activation. Oxid Med Cell Longev. 2015;2015:407580. (PubMed)
13. Higdon JV, Delage B, Williams DE, Dashwood RH. Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis. Pharmacol Res. 2007;55(3):224-236. (PubMed)
14. Coles BF, Kadlubar FF. Detoxification of electrophilic compounds by glutathione S-transferase catalysis: determinants of individual response to chemical carcinogens and chemotherapeutic drugs? Biofactors. 2003;17(1-4):115-130. (PubMed)
15. Seow A, Shi CY, Chung FL, et al. Urinary total isothiocyanate (ITC) in a population-based sample of middle-aged and older Chinese in Singapore: relationship with dietary total ITC and glutathione S-transferase M1/T1/P1 genotypes. Cancer Epidemiol Biomarkers Prev. 1998;7(9):775-781. (PubMed)
16. Dyba M, Wang A, Noone AM, et al. Metabolism of isothiocyanates in individuals with positive and null GSTT1 and M1 genotypes after drinking watercress juice. Clin Nutr. 2010;29(6):813-818. (PubMed)
17. Gasper AV, Al-Janobi A, Smith JA, et al. Glutathione S-transferase M1 polymorphism and metabolism of sulforaphane from standard and high-glucosinolate broccoli. Am J Clin Nutr. 2005;82(6):1283-1291. (PubMed)
18. Steck SE, Gammon MD, Hebert JR, Wall DE, Zeisel SH. GSTM1, GSTT1, GSTP1, and GSTA1 polymorphisms and urinary isothiocyanate metabolites following broccoli consumption in humans. J Nutr. 2007;137(4):904-909. (PubMed)
19. Economopoulos KP, Sergentanis TN. GSTM1, GSTT1, GSTP1, GSTA1 and colorectal cancer risk: a comprehensive meta-analysis. Eur J Cancer. 2010;46(9):1617-1631. (PubMed)
20. Egner PA, Chen JG, Zarth AT, et al. Rapid and sustainable detoxication of airborne pollutants by broccoli sprout beverage: results of a randomized clinical trial in China. Cancer Prev Res (Phila). 2014;7(8):813-823. (PubMed)
21. Sergentanis TN, Economopoulos KP. GSTT1 and GSTP1 polymorphisms and breast cancer risk: a meta-analysis. Breast Cancer Res Treat. 2010;121(1):195-202. (PubMed)
22. Bryan HK, Olayanju A, Goldring CE, Park BK. The Nrf2 cell defence pathway: Keap1-dependent and -independent mechanisms of regulation. Biochem Pharmacol. 2013;85(6):705-717. (PubMed)
23. Traka MH. Chapter nine – Health benefits of glucosinolates. Advances in Botanical Research. 2016;80:247-279.
24. Nothlings U, Schulze MB, Weikert C, et al. Intake of vegetables, legumes, and fruit, and risk for all-cause, cardiovascular, and cancer mortality in a European diabetic population. J Nutr. 2008;138(4):775-781. (PubMed)
25. Wang X, Ouyang Y, Liu J, et al. Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysis of prospective cohort studies. BMJ. 2014;349:g4490. (PubMed)
26. Zhang X, Shu XO, Xiang YB, et al. Cruciferous vegetable consumption is associated with a reduced risk of total and cardiovascular disease mortality. Am J Clin Nutr. 2011;94(1):240-246. (PubMed)
27. Joshipura KJ, Hung HC, Li TY, et al. Intakes of fruits, vegetables and carbohydrate and the risk of CVD. Public Health Nutr. 2009;12(1):115-121. (PubMed)
28. Cornelis MC, El-Sohemy A, Campos H. GSTT1 genotype modifies the association between cruciferous vegetable intake and the risk of myocardial infarction. Am J Clin Nutr. 2007;86(3):752-758. (PubMed)
29. Armah CN, Derdemezis C, Traka MH, et al. Diet rich in high glucoraphanin broccoli reduces plasma LDL cholesterol: Evidence from randomised controlled trials. Mol Nutr Food Res. 2015;59(5):918-926. (PubMed)
30. Liu B, Mao Q, Lin Y, Zhou F, Xie L. The association of cruciferous vegetables intake and risk of bladder cancer: a meta-analysis. World J Urol. 2013;31(1):127-133. (PubMed)
31. Yao B, Yan Y, Ye X, et al. Intake of fruit and vegetables and risk of bladder cancer: a dose-response meta-analysis of observational studies. Cancer Causes Control. 2014;25(12):1645-1658. (PubMed)
32. Vieira AR, Vingeliene S, Chan DS, et al. Fruits, vegetables, and bladder cancer risk: a systematic review and meta-analysis. Cancer Med. 2015;4(1):136-146. (PubMed)
33. Xu C, Zeng XT, Liu TZ, et al. Fruits and vegetables intake and risk of bladder cancer: a PRISMA-compliant systematic review and dose-response meta-analysis of prospective cohort studies. Medicine (Baltimore). 2015;94(17):e759. (PubMed)
34. Liu X, Lv K. Cruciferous vegetables intake is inversely associated with risk of breast cancer: a meta-analysis. Breast. 2013;22(3):309-313. (PubMed)
35. Wu QJ, Yang Y, Vogtmann E, et al. Cruciferous vegetables intake and the risk of colorectal cancer: a meta-analysis of observational studies. Ann Oncol. 2013;24(4):1079-1087. (PubMed)
36. Tse G, Eslick GD. Cruciferous vegetables and risk of colorectal neoplasms: a systematic review and meta-analysis. Nutr Cancer. 2014;66(1):128-139. (PubMed)
37. Bandera EV, Kushi LH, Moore DF, Gifkins DM, McCullough ML. Fruits and vegetables and endometrial cancer risk: a systematic literature review and meta-analysis. Nutr Cancer. 2007;58(1):6-21. (PubMed)
38. Wu QJ, Yang Y, Wang J, Han LH, Xiang YB. Cruciferous vegetable consumption and gastric cancer risk: a meta-analysis of epidemiological studies. Cancer Sci. 2013;104(8):1067-1073. (PubMed)
39. Lam TK, Gallicchio L, Lindsley K, et al. Cruciferous vegetable consumption and lung cancer risk: a systematic review. Cancer Epidemiol Biomarkers Prev. 2009;18(1):184-195. (PubMed)
40. Wu QJ, Xie L, Zheng W, et al. Cruciferous vegetables consumption and the risk of female lung cancer: a prospective study and a meta-analysis. Ann Oncol. 2013;24(7):1918-1924. (PubMed)
41. Han B, Li X, Yu T. Cruciferous vegetables consumption and the risk of ovarian cancer: a meta-analysis of observational studies. Diagn Pathol. 2014;9:7. (PubMed)
42. Hu J, Hu Y, Hu Y, Zheng S. Intake of cruciferous vegetables is associated with reduced risk of ovarian cancer: a meta-analysis. Asia Pac J Clin Nutr. 2015;24(1):101-109. (PubMed)
43. Li LY, Luo Y, Lu MD, Xu XW, Lin HD, Zheng ZQ. Cruciferous vegetable consumption and the risk of pancreatic cancer: a meta-analysis. World J Surg Oncol. 2015;13:44. (PubMed)
44. Liu B, Mao Q, Cao M, Xie L. Cruciferous vegetables intake and risk of prostate cancer: a meta-analysis. Int J Urol. 2012;19(2):134-141. (PubMed)
45. Zhao J, Zhao L. Cruciferous vegetables intake is associated with lower risk of renal cell carcinoma: evidence from a meta-analysis of observational studies. PLoS One. 2013;8(10):e75732. (PubMed)
46. Liu B, Mao Q, Wang X, et al. Cruciferous vegetables consumption and risk of renal cell carcinoma: a meta-analysis. Nutr Cancer. 2013;65(5):668-676. (PubMed)
47. Song JW, Chung KC. Observational studies: cohort and case-control studies. Plast Reconstr Surg. 2010;126(6):2234-2242. (PubMed)
48. Joseph MA, Moysich KB, Freudenheim JL, et al. Cruciferous vegetables, genetic polymorphisms in glutathione S-transferases M1 and T1, and prostate cancer risk. Nutr Cancer. 2004;50(2):206-213. (PubMed)
49. Spitz MR, Duphorne CM, Detry MA, et al. Dietary intake of isothiocyanates: evidence of a joint effect with glutathione S-transferase polymorphisms in lung cancer risk. Cancer Epidemiol Biomarkers Prev. 2000;9(10):1017-1020. (PubMed)
50. Wu QJ, Yang G, Zheng W, et al. Pre-diagnostic cruciferous vegetables intake and lung cancer survival among Chinese women. Sci Rep. 2015;5:10306. (PubMed)
51. Kirsh VA, Peters U, Mayne ST, et al. Prospective study of fruit and vegetable intake and risk of prostate cancer. J Natl Cancer Inst. 2007;99(15):1200-1209. (PubMed)
52. Richman EL, Carroll PR, Chan JM. Vegetable and fruit intake after diagnosis and risk of prostate cancer progression. Int J Cancer. 2012;131(1):201-210. (PubMed)
53. Nechuta S, Caan BJ, Chen WY, et al. Postdiagnosis cruciferous vegetable consumption and breast cancer outcomes: a report from the After Breast Cancer Pooling Project. Cancer Epidemiol Biomarkers Prev. 2013;22(8):1451-1456. (PubMed)
54. Fenwick GR, Heaney RK, Mullin WJ. Glucosinolates and their breakdown products in food and food plants. Crit Rev Food Sci Nutr. 1983;18(2):123-201. (PubMed)
55. Felker P, Bunch R, Leung AM. Concentrations of thiocyanate and goitrin in human plasma, their precursor concentrations in brassica vegetables, and associated potential risk for hypothyroidism. Nutr Rev. 2016;74(4):248-258. (PubMed)
56. McMillan M, Spinks EA, Fenwick GR. Preliminary observations on the effect of dietary brussels sprouts on thyroid function. Hum Toxicol. 1986;5(1):15-19. (PubMed)
57. Cho YA, Kim J. Dietary factors affecting thyroid cancer risk: a meta-analysis. Nutr Cancer. 2015;67(5):811-817. (PubMed)
58. US Department of Health and Human Services and US Department of Agriculture. 2015-2020 Dietary Guidelines for Americans. 8th ed.; 2015.
59. Traka MH, Saha S, Huseby S, et al. Genetic regulation of glucoraphanin accumulation in Beneforte broccoli. New Phytol. 2013;198(4):1085-1095. (PubMed)
News Update: Can Kale Cause Hypothyroidism?
The vegetable du jour kale has been getting negative attention in the media recently. Despite kale’s many nutritional benefits—including calcium, vitamin C, iron, fiber, and antioxidants—there is speculation that kale might be a contributor to hypothyroidism (an underactive thyroid). To uncover whether there is truth to this theory or the media is making much ado about nothing, EndocrineWeb spoke with Angela M. Leung, MD, who is an endocrinologist and Clinical Assistant Professor of Medicine at UCLA David Geffen School of Medicine, Los Angeles, CA, and Chair of the Public Health Committee at the American Thyroid Association.
Kale is considered a goitrogenic food, meaning that it contains substances (goitrogens) that may contribute to an enlarged thyroid. In fact, all cruciferous vegetables like kale are considered goitrogenic, including arugula, bok choy, broccoli, brussel sprouts, cabbage, cauliflower, collard greens, mustard greens, turnips, and watercress.
These vegetables “contain the substance thiocyanate, which in very high concentrations, can interfere with adequate iodine nutrition,” Dr. Leung said. The thyroid needs iodine to produce thyroid hormone, and “thus exposure to very high amounts of thiocyanate can potentially result in hypothyroidism (an underactive thyroid) and compensatory growth of the thyroid (goiter),” Dr. Leung explained.
“For the general population, the many health benefits of eating kale and other cruciferous vegetables in usual amounts far outweigh any potential adverse risks to the thyroid,” Dr. Leung said. “In usual amounts, kale consumption is healthy and should not be avoided, in contrast to some media reports which caution against all ingestion of cruciferous vegetables to promote thyroid health,” she said.
In people who already have a thyroid condition, “The risks of worsening a preexisting thyroid condition are likely minimal if goitrogenic foods are consumed in their usual amounts,” Dr. Leung said. “Patients should seek the advice of their physician for the proper management of their specific thyroid conditions,” she added.
How Much Kale Can You Safely Eat?
“The thiocyanate content of kale has not been well-studied, and there are only sparse measurement data from limited reports,” Dr. Leung said. “As such, the exact amount of kale ingestion that may be associated with an adverse thyroid health risk is unknown. However, ingestion of kale—including raw kale—in usual amounts should be fine,” Dr. Leung said.
In some reports in the press, juicing kale is the real culprit. “Although it has not been specifically studied, juicing kale concentrates the vegetable and thus potentially poses a greater risk toward iodine deficiency and hypothyroidism if ingested in large amounts on a very frequent basis,” Dr. Leung said. “These risks may be exacerbated in individuals who are already iodine deficient, and these may include those with restricted diets, such as vegetarians and vegans,” she said.
The United States is considered generally iodine sufficient, as most people get enough iodine through their diet, from table salt (of which most, but not all, formulations have iodine added to it), and from iodine-containing multivitamins and supplements, Dr. Leung noted. “However, adequate iodine nutrition is particularly important in women of child-bearing age and their children, given the importance of iodine and normal thyroid function on the developing brain in young infants. The daily recommended intake for iodine is 150 mcg (micrograms), and women who are contemplating pregnancy, pregnant, or lactating should supplement with a multivitamin containing 150 mcg daily. It should be noted that iodine excess is also potentially dangerous, as it can similarly induce thyroid dysfunction, and ingestion of any supplement containing more than 500 mcg iodine per day should be avoided,” she said.
Thus, media reports of kale causing hypothyroidism does not seem likely in most cases. Eating greens in their usual amounts will not be a significant contributor toward thyroid disorders. As always, it is important to talk to your doctor regarding your individual risk for a thyroid disorder and what types of food are right for you.
Sources
1. Paxman PJ and Hill R. The goitrogenicity of kale and its relation to thiocyanate content. J Sci Food Agric. 1974;25(3):329-337.
2. Chandra AK, Singh LH, Ghosh S, Pearce EN. Role of bamboo-shoot in the pathogenesis of endemic goiter in Manipur, northeast India. Endocr Pract. 2013;19(1):36-45.
3. Public Health Committee of the American Thyroid Association, Becker DV, Braverman LE, Delange F, et al. Iodine supplementation for pregnancy and lactation – United States and Canada: Recommendations of the American Thyroid Association. Thyroid. 2006;16(10):949-951.
4. ATA Statement on the Potential Risks of Excess Iodine Ingestion and Exposure. Accessed July 7, 2014. Available at: http://www.thyroid.org/ata-statement-on-the-potential-risks-of-excess-iodine-ingestion-and-exposure/
Updated on: 03/16/16
Hypothyroidism in Children
Goitrogens – an overview | ScienceDirect Topics
12 Goitrogens and Thyroid Function
Certain dietary factors, the goitrogens, are believed to limit the ability of the body to utilize iodine. Goitrogenic foods include (1) cruciferous vegetables (i.e., broccoli, kale, and cabbage) that contain thioglucosides, which are metabolized to thiocyanates and inhibit iodine uptake from the thyroid gland, (2) sweet potatoes, cassava, and lima beans, which contain cyanogenic glucosides that may be metabolized into thiocyanates as well, and (3) soy products and millet, which contain flavonoids, believed to have “antithyroid” activity via thyroperoxidase inhibition (it is not clear whether it is soy/millet flavonoids that exert this activity or all flavonoids), contributing to the genesis of endemic goiter (Gaitan, 1990, 1996). Drinking water and eating foods that contain perchlorate may inhibit of iodine uptake by the thyroid. Some of these factors will be relevant to the vegetarian diets.
In a cross-sectional study of ovolactovegetarians and vegans in Boston, no significant association between UI, perchlorate, and thiocyanate concentrations and thyroid function were found (Leung et al., 2011). In a cross-over study in the United Kingdom, short term high goitrogenic food intake in a population with marginal iodine intake did not impact thyroid function (Bouga et al., 2015). More recently, an association was demonstrated in a subsample of the Adventist Health Study (AHS-2), between soya isoflavone intakes and higher odds of high TSH concentrations in women only (OR 4·17, 95% CI 1·73, 10·06) but not in men (OR 1·05, 95% CI 0·27, 4·07) (Tonstad et al., 2015a). As just over half of the sample had UI concentration below 100 μg/L, it is possible that soy isoflavones exert an effect on thyroid function when iodine status is insufficient. Genistein aglycone, a soy-derived isoflavone, did not affect thyroid function (TSH, free T3, free T4) after 3 years of treatment in postmenopausal women (Bitto et al., 2010), in accordance with the results of a 6-month study that used isoflavone supplements (Bruce et al., 2003). It is perhaps important to point out that the iodine intake or excretion of these populations was not evaluated, and the outcomes may be a function of the iodine status.
The relationship between cruciferous vegetables (goitrogenic, and enriched in vegetarian diets) is not clear. Dal Maso points to a nonsignificant relationship between cruciferous vegetable intake and thyroid cancer (RR = 0.9, 95% CI: 0.8–1.1) (Dal Maso et al., 2009). Meanwhile, a case–control study in New Caledonia found an increased association between consumption of cruciferous vegetables and odds of thyroid cancer, but again only in women with low iodine intake (Truong et al., 2010). There are studies, though, that have focused on goitrogens intake from the diet.
90,000 Who needs seaweed? | HEALTH: Events | HEALTH
Therefore, one should not be limited only to eating a large amount of seaweed, the use of iodized salt and assume that this will insure against all problems.
The thyroid gland produces hormones in our body that affect the metabolism, and through it – on the growth of bone tissue, brain development, decomposition of cholesterol and fats, on blood circulation and psyche. The most common disorders in her work are increased (hyperthyroidism) or decreased (hypothyroidism) production of these hormones.But changes in the structure of thyroid tissue are much more common than violations of its function. The gland can become enlarged, nodules or cavities filled with fluid (cysts) can form in it.
An enlarged thyroid gland, or euthyroid goiter, manifests itself in hormonal changes and an increased need for iodine. It is especially common in adolescents during puberty and in women during pregnancy and lactation. These risk groups also include all people living in regions where there is a natural lack of iodine and there is no prevention of iodine deficiency.There are effective treatments for virtually all thyroid disorders today.
… If collar presses
With an enlargement of the thyroid gland at the first stage, the goiter can be palpated. The enlargement of the gland does not manifest itself clinically, just a feeling of pressure, difficulty in swallowing, shortness of breath during exertion or a certain position of the head. Sometimes it seems that the collar of a shirt or blouse has become too tight. In the second stage, the goiter can be seen and palpated in the normal position of the head.In the third stage, it is visible from a distance.
If the frequency of thyroid gland diseases in the family is 50%, or you have discovered some unfavorable symptoms, you need to go to an endocrinologist. In about 40% of cases, the diagnosis can only be made by clinical examination. Ultrasound allows you to determine not only the volume of the gland, but also gives information about its change. It is also necessary to be tested for thyroid hormones, antibodies to thyroid tissue. In some cases, patients over 40 years of age with nodular goiter with suspected malignant tumors and for the diagnosis of inflammation need a special study – scintigraphy (a radioisotope preparation is injected and a two-dimensional picture of internal organs is examined).
Iodine is not always needed
There can be many reasons for goiter, therefore treatment can be varied. In no case do not try to compensate for the lack of iodine with drugs on your own. It can hurt.
Tableted forms of iodine should be prescribed by a doctor after examination, because first it is necessary to exclude autoimmune processes in the thyroid gland (for example, autoimmune thyroiditis, which is accompanied by a decreased or increased thyroid function).In such cases, iodine can aggravate the course of the disease. Iodine-containing preparations are contraindicated for thyroid neoplasms, after thyroid surgeries and for other diseases.
See also:
90,000 Cabbage and thyroid glands. Should you be afraid of goitrogens? – ET
Cabbage vegetables are rich in nutrients including vitamin C, vitamin K, vitamin B complex and carotenoids. Photo: jcesar2015 / pixabay / CC0 Public Domain
Today I want to talk to you about one of my favorite topics: thyroid health.If we talk about the thyroid gland, one cannot but touch upon the issue of cabbage vegetables. /epochtimes.ru/
Vegetables of the cabbage family … It is difficult to refute the value of broccoli and its brothers in the family. But I know that you can find conflicting information about these healthy beauties, especially when it comes to thyroid health.
What are cabbages?
When we talk about the cabbage family, we mean the following green vegetables:
- Broccoli
- Kale, or kale
- Brussels sprouts
- Cauliflower
- Collard greens
- Mustard
- Arugula
- Bok Choy
- Peking cabbage
- Some root vegetables – radishes, turnips, horseradish and wasabi
Cabbage vegetables are rich in nutrients, including vitamin C, vitamin K, vitamin B complex, and carotenoids.
I remember listening to a friend and colleague speaking at a meeting dedicated to the treatment of Hashimoto’s disease a few years ago. He talked about how few people are likely to be able to eat enough of these vegetables every day to reap the health benefits reported in research on cancer.
However, what is good for one person can be bad for another.
You may have heard that the goitrogens in these vegetables can do more harm than good for people with thyroid disease.
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What are goitrogens?
Curiously, these very healthy cabbage family foods contain goitrogens, which can cause thyroid hormone deficiency. This can happen in the following cases:
- with excessive use;
- in case of iodine deficiency in the body;
- in case of excess calcium and fluorine.
Many doctors, including renowned thyroid health experts, say it is nearly impossible to consume enough goitrogens to cause a real problem.
This can happen if you only eat turnips and rutabagas every day as a main course and at the same time have a lack of iodine in the body.
Of course, each of us is unique. Each person has an individual supply of minerals and their lack. Different people benefit or harm from the same food.
Since cabbage vegetables are rich in antioxidants and fiber, and this is beneficial for many diseases, I do not recommend refraining from them. And I say this as a person with a thyroid disease, who has learned to keep the disease under control and teaches other people to do this.
You may have heard that cooking helps to detoxify goitrogens in cabbage vegetables, and this is true. However, there is no data on what the temperature and processing time of food should be in order to achieve such an effect.
To be cabbage
Still, cooking and moderation will allow you to benefit from these vegetables and not be afraid of harm.
As I said before, I love all vegetables of the cabbage family, especially for their beneficial effects on the liver.
These vegetables are an almost unrivaled food activator of glutathione (the king of all antioxidants). They stimulate the elimination of many toxic chemicals through the liver.
There is a lot of information to learn to understand what to eat and how to meet our individual nutritional needs. Despite the differences, I love that we can do this together.
English version
What if the thyroid gland begins to malfunction? Endocrinologist Tips
Frightening figures are cited by experts from the World Health Organization.According to them, in Russia more than 20 million people suffer from thyroid diseases. This is due to the lack of trace elements, and constant stress, and the frantic pace of life. But it is this organ that is responsible for human immunity.
Report by Tatiana Ionova.
Lyubov Cheban felt unwell for a long time, but attributed it to fatigue. And sore throat – for a cold. Six months ago, during the clinical examination, it was discovered that she had an enlarged thyroid gland. She did not receive treatment, she decided to go away by herself.Now there is only one way – operation.
Lyubov Cheban: “I sleep very badly now. That is, there is very little sleep at night compared to how it used to be and now. And now the suffocation is coming. That is, I can’t sleep on my back, I feel bad.”
It looks like a butterfly – this little organ with a mission – to regulate the entire metabolism in the body. And in a healthy state it is practically not palpable. The main cause of the disease is a lack of iodine, doctors say, and the best prevention is iodized salt and seafood in the daily diet.But today the average Russian consumes only 80 micrograms of this mineral per day, at a rate of two hundred. Iodine deficiency is especially dangerous for children and pregnant women.
Svetlana Usova: “The fact is that I love salty, but that does not mean that I eat iodized salt. I am just arriving in the region of the Caucasian Mineral Waters. There, basically, I used not iodized salt, although I know very well what it would be desirable to use “.
According to statistics, women suffer from thyroid gland diseases 8 times more often than men and usually develop between the ages of 30 and 50.Photos from the beginning of the last century. A goiter the size of a tennis ball was common. So in many countries with a shortage of iodine, laws have been passed on the mandatory use of iodized salt. Including in the USSR in 1953, and it seemed that the problem remained in the past. And here comes the splash again.
Yekaterina Troshina, endocrinologist, FGU ESC RAMS: “If we recall the experience of the Soviet Union, then at that time almost all residents of that country received iodized salt, because the corresponding orders of the Ministry of Health were in force.Nobody just thought about what kind of salt he was eating. But now we have market relations, different manufacturers, different views, so now there is a so-called voluntary model of this prevention. “
But thyroid diseases can occur for other reasons. Risk factors – stress and heredity. to start producing either too many hormones and the person suddenly loses weight, does not tolerate heat well, complains of trembling in his hands, or vice versa – if there are not enough hormones, the patient is constantly freezing, wants to sleep, and quickly overtired.And it is always a blow to the nervous system.
Elena Semenova, neurologist, FGU ESC RAMS: “Damage to the central nervous system is manifested, among other things, in hyperthyroidism, irritability, irascibility, anxiety, trembling.”
Valery knew that he had problems with the thyroid gland, refused to be treated – he was admitted with a suspicion of a heart attack. If the disease is started, most often the heart is at risk. To avoid serious complications, doctors advise at the first suspicion to contact an endocrinologist.And the most important thing is to start treatment as early as possible. Only in this case, experts say, you can not only avoid the operation, but also return to a full life.
Guest in the studio – Galina Melnichenko, Doctor of Medical Sciences
Presenter: “The key to the health of the whole body” – this is how doctors called the thyroid gland in the 19th century. So what to do if she suddenly starts bothering you? We will talk about this with Galina Melnichenko, Doctor of Medical Sciences, Professor of the Department of Endocrinology at the Sechenov Moscow Medical Academy.Hello Galina Afanasyevna.
Guest: Good afternoon.
Presenter: Tell me, can a person himself understand that the thyroid gland is really out of order?
Guest: In some cases it can. In some, he cannot and cannot even suspect. In some, he mistakenly suspects that the thyroid gland is out of order.
Presenter: Is it considered that one of the main signs of a diseased thyroid gland is a lump on the neck?
Guest: I would not say a seal, I would say an increase.But no matter how much we talk about changing the shape, the worst thing is a change in the function of the thyroid gland. Changes in form and change in function do not always run in parallel. Increased activity is more terrible. It is easier to control and correct an underactive thyroid gland.
Presenter: And in what years do you need to pay special attention to your health and maybe additionally do some analyzes, get checked?
Guest: The most important thing is newborns. Everyone is required here.And the second time is pregnancy. Between 8 and 12 weeks of pregnancy, check the functioning of the thyroid gland. Her poor performance can affect a child’s intelligence and development. In the future, after 35 years, once every 5 years, check the state of the thyroid gland on purpose, over 50 years – check at intervals of a year or two.
Presenter: Maybe it’s worth taking and drinking some iodine-containing vitamins in advance, or maybe it’s worth picking up on seaweed?
Guest: Let’s leave the seaweed aside for now.The world has long created a simple model of silent prevention of iodine deficiency. Here salt was chosen as a silent carrier. That is, the housewife who runs the household should buy mainly iodized salt. And cook on it.
Presenter: As for seaweed, why did you say that it needs to be discussed separately?
Guest: Imagine for a second that you have to buy seaweed day after day, the iodine content of which is not controlled by anyone. If seaweed is your favorite dish beautifully, then the question arises – why did the countries located near the sea still adopt a law on the universal iodization of salt?
Presenter: That is, after all, salt iodization is more useful and more important?
Guest: It’s not even more useful, it’s just an indispensable element of normal European cultural life.Only and only.
Presenter: If, nevertheless, trouble happened, thyroid problems were discovered, what kind of treatment is usually prescribed to a person? Is it outpatient or inpatient?
Guest: It depends on what kind of disease you are talking about. The vast majority of them, even if they require treatment, this treatment is not overly complicated, overly expensive, and it ensures a completely normal life.
Presenter: Thank you, Galina Afanasyevna. What rules must be observed in order to never have problems with the thyroid gland and in what cases it is impossible to postpone a visit to the doctor, the doctor of medical sciences, professor of the Department of Endocrinology of the Sechenov Moscow Medical Academy Galina Melnichenko told us about this.Well, now let’s summarize our conversation.
One of the main causes of thyroid diseases is iodine deficiency. Severe stress, infections and poor heredity can also provoke ailment.
Constant fatigue, heart palpitations and drowsiness will tell you that there are problems with the thyroid gland. It is worth paying attention to this organ with a sharp change in weight and with increased pressure.
It is necessary to consult a doctor if you find a lump or swelling in the neck area, as well as if the shape of the eyes has changed.With diseases of the thyroid gland, they are unnaturally enlarged – as if from surprise.
For the prevention of thyroid diseases, doctors advise to eat more foods with a high iodine content. We are talking about sea fish, seaweed and, of course, iodized salt.
Check the condition of the thyroid gland regularly – once every two years. First of all, this applies to people over 50. The condition of your thyroid gland can be found out by a blood test for hormones or by doing an ultrasound of the neck.
The doctor told about the most useful product for the thyroid gland and immunity
Seaweed has a lot of useful properties, but the main thing is that it helps to strengthen the immune system and normalize the thyroid gland.
In autumn, due to sudden changes in the weather and malfunctioning of the thyroid gland, the immune system turns out to be unstable, it is important to eat fully and balanced and fill the deficiency of vitamins and nutrients in order to help your body fight inflammation. Nutritionist Rimma Moysenko told about which product will help strengthen the immune system and make up for the lack of nutrients.
What does the thyroid gland have to do with it?
The thyroid gland is responsible for stimulating the cells of the immune system, this is one of its main functions.To normalize the thyroid gland, it is necessary to consume large amounts of water and foods that contain iodine. However, many experts note that in many regions of our country there is a shortage of this vital substance in water. According to the nutritionist, iodine deficiency is bad for the thyroid gland, which is responsible for our mood, performance and immune protection, but if it cannot be obtained with every fluid intake, then it will be possible to make up for its deficiency with the help of a simple product that can definitely be found in any supermarket.
Where is iodine?
So, the required dose of iodine is contained in seaweed. This product is a storehouse of useful substances and minerals, so you should not bypass it, especially in the autumn. To protect the body from thyroid malfunction and a weakened immune system, you need to add seaweed to your daily diet. Fortunately, it tastes very good and is suitable for every meal – as a separate dish or as a side dish. By consuming the product in large quantities, you can significantly improve the immune system, the expert noted.
General recommendations
According to the recommendations of Rimma Moysenko, the most useful seaweed is fermented, however, in dried form, it also contains a sufficient amount of iodine for the body. In order not to be mistaken in choosing a product, the specialist advised buying cabbage of the darkest color. “The darker the seaweed, the more iodine it contains,” concluded the nutritionist.
However, before eating cabbage for preventive purposes and trying to strengthen the immune system with other foods, you should consult your doctor, because in some cases, such self-medication can be dangerous.
THYROID DIET | Science and Life
The thyroid gland is located near the front of the neck, just below the thyroid cartilage. It resembles a butterfly in shape.
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The thyroid gland is one of the largest endocrine glands: in an adult it weighs 15-20 g and consists of two lobes 4 cm long and 2-2.5 cm wide, connected by an isthmus. It owes its name to the anatomical proximity to the cartilage of the larynx, which resembles a shield in outline.Sometimes the thyroid gland may not be located behind the cartilage, but, for example, at the root of the tongue or behind the sternum. For some people, it is completely absent. If earlier babies born without a thyroid gland were doomed, now synthetic hormonal drugs completely compensate for the absence of natural thyroid hormones in the blood.
The purpose of the gland is to produce thyroid hormones: thyroxine and triiodothyronine. For the normal functioning of the thyroid gland, iodine is absolutely necessary, since it is part of the hormones: thyroxine contains four iodine atoms, and triiodothyronine – two.The body cannot synthesize iodine on its own, we get it exclusively with food.
What happens if there is not enough iodine in food? To capture more iodine, the thyroid gland begins to grow – the number and volume of thyroid cells increases, – a goiter is formed. So the body compensates for the lack of iodine. But if the iodine deficiency persists long enough, an increase in the volume of the gland does not normalize iodine intake and symptoms of iodine deficiency appear.
Thyroid hormones regulate the growth and development of cells, the functions of the central and peripheral nervous systems, muscular, reproductive, bone, cardiovascular, respiratory and other systems of the body. And most importantly, they can control the processes of protein synthesis. Another very important effect of the action of thyroid hormones is the ability to stimulate cellular and tissue respiration in mitochondria. Therefore, iodine deficiency leads to serious consequences: mental abilities decrease, apathy and drowsiness appear, and metabolism is disturbed.
Throughout his life, a person consumes only 3-5 g of iodine. Iodine as a trace element is a part of many natural organic compounds or is present in inorganic salts in the form of iodide anion. 10-20% of the total iodine intake is selectively absorbed by the thyroid gland, in which 6000-8000 mcg is usually concentrated. In the blood, 500-600 μg of iodine circulates. Every day, the thyroid gland spends 75 mcg of iodine for the needs of the body. The daily requirement of the whole body is 100-200 mcg of iodine, depending on age and state of health.Endocrinologists recommend the following iodine intake rates:
children from 2 to 6 years old – 90 mcg;
children from 7 to 12 years old – 120 mcg;
adults 12 years and older – 150 mcg;
pregnant and lactating women – 200 mcg.
Thus, the largest amount of iodine is required by pregnant women. This is not surprising: thyroid hormones are necessary for the development of the fetus. The fetal thyroid gland begins to work from the 12th week of pregnancy, therefore the first three months the embryo develops exclusively due to the mother’s thyroid hormones.If they are not enough, the whole organism of the unborn child suffers, and above all his brain. In addition, iodine deficiency is dangerous for the mother, as the body’s intake of iodine increases during pregnancy. This means that a lack of it in the food of a pregnant woman can lead to the rapid development of goiter.
Almost the entire population of the Russian Federation, with the exception of residents of the sea coasts,
lives in areas with mild, moderate and severe natural iodine deficiency.
But this is not the only reason for the development of thyroid diseases.In vegetables,
belonging to the cruciferous family, contains organic compounds
with SCN group: thiocyanates and isothiocyanates. This family includes white cabbage,
Brussels sprouts and cauliflower, broccoli, turnips, horseradish, watercress. Proven
that thiocyanates and isothiocyanates – substances that contribute to the development of goiter – are goiters. Another group of food goobogens are products containing substances – precursors of thiocyanates. These include cassava, corn, sweet potatoes, beans, and maize.Coal, shale, household and industrial waste, chemical fertilizers and pesticides have goitrogenic properties. Thiocyanates are also found in tobacco. All these products disrupt the synthesis of thyroid hormones, exacerbating the natural iodine deficiency.
You can fill the lack of iodine in different ways. The most effective and economical method is the iodization of table salt and bread. This method of prevention is called “mute”: a person often does not know that he is eating a food product enriched with iodine.At present, a new standard has been adopted in Russia, which involves the addition of 40 ± 15 mg of iodine per kilogram to table salt. The use of iodized table salt in many cases can eliminate iodine deficiency. However, at certain periods of life (children and adolescents, pregnancy, breastfeeding), the body needs regular additional intake of physiological doses of iodine. In such cases, drugs are prescribed containing a physiological dose of potassium iodide, for example, Iodomarin, one tablet of which contains a daily dose of iodine.
Is there another way to normalize iodine levels? Of course, if you eat oysters, trepangs, squid, seaweed and scallops every day, as the Japanese do. They consume up to 1500 mcg of iodine per day and do not get goiter. In our conditions, it is most advisable to regularly use iodized salt, as the Austrians, Swiss, French, living in conditions of severe natural iodine deficiency do, and to take Iodomarin.
About the thyroid gland – Dialogue online pharmacy
The thyroid gland produces several hormones at once, thereby controlling all vital processes in our body.Starting from the metabolic rate and ending with the efficiency of the heart.
Disruption of her activity can lead to improper production of hormones, which, in turn, will cause poor health, increased emotionality and disruption of vital processes.
Severe hair loss and loss of hair quality is one of the symptoms of thyroid problems. So, if you begin to notice that a good part of your hairstyle remains on your comb in the morning, then maybe it is worth contacting a specialist?
You probably remember how, as a child, we were shoved with seaweed, convinced that it would help our thyroid gland.Of course, we didn’t have to worry about health at that age, and the cabbage happily passed our stomachs.
In this article, we’ll go over some tips to help you keep your thyroid healthy!
Seaweed
Of course, you can’t go without it! Seaweed, like other seafood, contains iodine. Which is so necessary for the effective functioning of the thyroid gland.At the same time, it can be consumed not only in food, but also in the form of tablets. However, an endocrinologist should be consulted before treatment.
Avoid soy
Consuming soy products (miso and tofu) as a supplement to your main food may not harm your body in any way. However, having too many supplements and foods that contain soy isoflavones in your life can have a negative impact on your thyroid function.
Study labels in detail
Particular attention should be paid to supplements that are aimed at improving and alleviating the menopause process. Most often, soy isoflavones are found in them.
Avoid starch and refined sugar
This recommendation is focused mainly on maintaining the overall health of the body. Foods high in sugar allow your body to fill up without replenishing the supply of nutrients it needs to function.
And if your thyroid gland does not receive enough nutrients, then you can forget about its normal functioning!
Exercise regularly
Regular exercise helps improve blood circulation in the body. And this leads to the fact that the thyroid gland works as efficiently as possible, because it does not lack the substances necessary for vital activity!
However, it is important to understand that a couple of squats a day is not enough.It is important to engage in physical activity regularly, this is the only way you can achieve the desired result!
We hope our tips will help you maintain your thyroid health. And your life will become much calmer and more pleasant!
Thyroid Health Products // Watch
The thyroid gland is responsible for the production of hormones necessary for normal metabolism, cell growth and the cardiovascular system.For the proper functioning of this organ, it is important that iodine enters the body. What foods contain the most of this substance? The answer is in the program “On the most important thing.”
The thyroid gland is responsible for hormones that are necessary for normal metabolism, cardiovascular system and cell growth. For its proper functioning, iodine needs to enter the body. On the air of the Russia 1 TV channel, Dr. Alexander Myasnikov explained which foods contain the maximum amount of iodine, and which foods should be discarded if you have been diagnosed with thyroid problems.
Diseases of the thyroid gland are insidious in that they can hide behind absolutely any symptoms. Fatigue, dizziness, increased blood pressure, sleep disturbances, a sudden change in weight – all this can be a signal from the thyroid gland. “All these symptoms indicate that you may have a lack of iodine. On average, we should consume 150 mcg of iodine per day. Pregnant women need more,” said Alexander Myasnikov.
In the program “On the most important”, the expert listed the products that must be included in the diet to prevent illness: fresh seafood, seaweed, spinach, eggs, dried fruits.
“Pay close attention to what you eat. Lack of iodine leads to the development of cretinism. And this is not a curse, as you might think, but the name of a serious endocrine disease caused by a lack of thyroid hormones. Cretinism is characterized by a delay in physical and mental development.” added the specialist.
Alexander Leonidovich also named products that are not recommended to be consumed in large quantities for thyroid problems: “Cauliflower, broccoli, soybeans are good for the heart and blood vessels, but not good for the thyroid gland.”
He urged everyone to stop smoking. It disrupts the production of thyroid hormones. In addition, certain medications can harm the thyroid gland. For example, taking amiadorone, a medication for arrhythmias, can lead to an excess of iodine in the thyroid gland.