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REVIEW ARTICLE
Year : 2014  |  Volume : 3  |  Issue : 2  |  Page : 60-65

Diet and thyroid - myths and facts


1 Department of Medicine, Command Hospital, Lucknow, Uttar Pradesh, India
2 Department of Psychiatry, Era Medical College, Lucknow, Uttar Pradesh, India
3 Department of Endocrinology, Command Hospital, Lucknow, Uttar Pradesh, India

Date of Web Publication6-May-2014

Correspondence Address:
K. V. S. Hari Kumar
Department of Endocrinology, Command Hospital, Chandimandir 134 107, Haryana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2278-019X.131954

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  Abstract 

Thyroid gland is located in the neck and synthesize thyroid hormones, which have an indispensable role in the metabolic functions of the body. Iodine is an essential compound for the synthesis of thyroid hormones and is mostly derived from the environment. Other important nutrients for the thyroid function include selenium, iron, Zinc and vitamin A. Dietary alterations of the micronutrients lead to structural and functional alterations in thyroid function. The alternative medical practitioners and nutritionists advocate plenty of dietary modifications without a scientific rationale. In this article, we review the role of dietary micronutrients in thyroid physiology and dispel few myths surrounding the same topic.

Keywords: Diet, goiter, hyperthyroidism, hypothyroidism, thyroid


How to cite this article:
Sharma R, Bharti S, Kumar KH. Diet and thyroid - myths and facts. J Med Nutr Nutraceut 2014;3:60-5

How to cite this URL:
Sharma R, Bharti S, Kumar KH. Diet and thyroid - myths and facts. J Med Nutr Nutraceut [serial online] 2014 [cited 2019 Jul 17];3:60-5. Available from: http://www.jmnn.org/text.asp?2014/3/2/60/131954


  Introduction Top


Thyroid gland is an important endocrine gland located in the neck and is the site for production of thyroid hormones. The synthesis of thyroid hormones is under the hypothalamus-pituitary control similar to other hormonal axes. Iodine is a major substrate for the synthesis of thyroid hormones and is derived mostly from the environment. [1] The relation of iodine and goiter is known for many centuries leading to the universal salt iodination program to limit the detrimental effects of iodine deficiency. [2] Previous observations also suggest the presence of goitrogenic substances in the diet, identifying an important role of dietary constituents in thyroidology. [3] Thyroid disorders are very common in the society, affecting about 10-15% of the population. Universal salt iodization helped in the prevention of goiter and other iodine deficiency disorders. The persistence of goiter even after the iodinization leads researchers to explore the relation of other dietary nutrients in the thyroid physiology. [4] The micronutrients other than iodine, which play important role in thyroid hormone synthesis are selenium, iron and zinc. [5] The alterations in the dietary components may lead to thyroid dysfunction in predisposed individuals. In this article, we shall review the relation between diet and thyroid and try to dispel certain myths on this subject.

Thyroid physiology and dietary constituents

The hormones secreted from the thyroid gland are thyroxine (T4) and tryiodothyronine (T3). T3 is the active hormone and T4 acts as the prohormone. Only 20% of T3 is secreted from the thyroid and rest 80% comes from T4 deiodination in peripheral organs like liver and kidney. [6] Thyroid hormone regulates metabolic rate, body temperature and tissue growth. The thyroid gland is made of follicles, which are surrounded by a single layer of epithelial cell called the follicular cell. Follicle absorbs iodine and stores it in thyrolobulin a glycoprotein synthesized within thyroid cells. The thyroid hormone synthesis can be summarized in the four steps. Firstly, active uptake of circulating iodide to cytosol by sodium iodide symporter, secondly, oxidation of iodide by thyroid peroxidase and iodination of tyrosine residues on thyroglobulin molecule, creating mono and diiodotyrosines, thirdly, coupling of iodinated tyrosine residues to form T3 and T4 and forthly the step of proteolysis due to hydrolysis and releasing the T3 and T4 in cytosol. Iodine remains the major nutrient required for the synthesis of thyroid hormones. The second important micronutrient is selenium, which forms selenocysteine compounds and protects the thyroid from free radical damage. [7] Research has shown that iron, vitamin A and zinc also plays an important part of thyroid hormone synthesis. [5] Hence, dietary intake of all these micronutrients is essential for the functioning of the thyroid gland.

Iodine and thyroid

Iodine is essential for the iodination of tyrosine residues leading to the formation of thyroid hormones. A detailed discussion on this topic is beyond the purview of this article and readers are requested to peruse the recently published reviews. [8],[9] Environmental iodine is the main source of iodine, that is present in soil, sea water, dairy products, seafood and eggs. Iodized salt and multivitamin tablets containing iodine are the other sources of iodine. Recommended dietary allowance for iodine for adult men and women is 150 ug and for pregnant and lactating women is 220 ug and 290 ug respectively. Urinary iodine level is the best measure to assess the iodine level in the body and iodine deficiency is diagnosed when the median iodine concentration is less than 50 ug/ml in population. [10] Iodine supplementation in the form of iodized salt and iodized oil has proven dramatic improvement in many developing countries. Certain population like pure vegetarian may not reach an adequate iodine intake even in countries considered iodine sufficient. A reduction in iodine intake can also be related to reduced salt intake for hypertension. Depending on availability of iodine, the thyroid gland is able to modify the use of iodine for thyroid hormone production. The failure of compensation in severely iodine deficient population results in hypothyroidism and developmental brain damage. In mild iodine deficiency, thyroid gland adapts by hyperfunctioning and prolonged hyperactivity leads to autonomous thyroid function.

Both the excess or deficient intake of iodine is associated with thyroid disorders in the population. [11] Iodine deficiency can lead to a variety of medical problems at all ages in the humans. Children of mothers having an iodine deficiency during pregnancy may have mental retardation, deaf mutism, spasticity and short stature. Congenital hypothyroidism due to iodine deficiency is the most common cause of preventable mental retardation in the world. [12] Other disorders include goiter, hypothyroidism and myalgia. Iodine deficiency in pregnant women is associated with miscarriage, stillbirth, preterm labor and congenital disorders in babies. The consumption of excess iodine is also associated with various thyroid disorders like hyperthyroidism, autoimmune thyroid disease and nodule formation. The safe upper limit of iodine intake is around 1.1 mg per day. One teaspoon of iodized salt contains 284 micrograms of iodine and a single gram of seaweed contains around 2 mg of iodine.

Selenium and thyroid

The thyroid gland is among the human tissues with the highest selenium content similar to other endocrine organs. Selenium is an integral part of selenoproteins and critical enzymes in thyroid hormone synthesis making this an essential micronutrient. [13] Selenoproteins (glutathione peroxidase and thioredoxin reductase) are responsible for the cellular antioxidative defense and protects the thyroid gland from damage due to hydrogen peroxide and reactive oxygen species. The key enzymes involved in the activation and inactivation of thyroid hormones (iodothyronine deiodinases) are also selenoproteins. Selenium deficiency exacerbates iodine deficiency and they both in combination contribute to the pathogenesis of hypothyroidism, goiter, autoimmune thyroid disease and myxedematous cretinism. [14] Selenium is found mainly in the soil and the consumption of balanced diet gives adequate selenium for thyroid hormone synthesis. The selenium rich foods in the diet are mushrooms, garlic, onions, eggs, beef liver, shellfish, wheat germ, sunflower seeds and sesame seeds. Selenium deficiency is seen in patients with poor gastrointestinal absorption, long term parenteral nutrition therapy and people residing in areas where the soil content is very low. Replacement of selenium is essential in these patients to prevent thyroid dysfunction. In patients with combined selenium and iodine deficiency, replacement of selenium alone worsens the condition further due to the peripheral conversion of T4 to T3 leading to a marked reduction in T4. Hence, in regions of combined iodine and selenium deficiency, iodine supplementation is mandatory prior to the initiation of selenium supplementation.

Iron and thyroid

Several minerals and trace elements including iron are essential for normal thyroid hormone metabolism. The thyroid function is impaired when the deficiency of these elements coexists in the body. Iron deficiency impairs the synthesis of thyroid hormones by reducing the activity of heme-dependent thyroid peroxidase. Population studies have revealed that nonanemic children responded swiftly to iodine supplementation with regard to goiter and TSH levels than anemic children. [15] Globally, iron and iodine deficiency coexist and the authorities have developed a double fortified salt (iodine and iron) to tackle the problem in an effective manner. [16]

Thyroid dysfunction and dietary alterations

The thyroid disorders may be divided clinically into four common syndromic presentations. They include hypothyroidism, hyperthyroidism, thyroid swelling (diffuse or nodule) and thyroid cancer. Each of these thyroid disorders has a relevant dietary alteration in the clinical course as explained below and summarized in [Figure 1].
Figure 1: Dietary advice for thyroid in health and disease

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Hypothyroidism and goitre

Iodine deficiency is the major cause for thyroid deficiency as explained in the previous sections. Previous reports suggest that a vegetarian diet was associated with reduced risk of hypothyroidism than omnivorous diets in population studies with a follow up of 6 years. [17] The presence of goitrogenic substances in the diet is responsible for the persistent goiter in post iodization phase. The goitrogenic substances in the normal human diet are the vegetables from the Brassica genus (Cauliflower, Cabbage, Broccoli, Horseradish, Radish, Rapeseed and Turnips), cassava, which contains cyanogenic glucosides, flavonoids and organic residues in the soil. [18] Cabbage and cauliflower have high concentrations of glucosinolates, bamboo shoot and cassava were rich in cyanogenic glucosides and other vegetables like mustard, turnip and radish are rich in thiocyanate content. All the goitrogenic substances affect the thyroid hormone synthesis by inhibiting the iodine uptake and the activity of thyroid peroxidase.

Excess iodine in the diet may lead to transient hypothyroidism, known as Wolff-Chaikoff's effect. [19] This autoregulation of the thyroid hormone synthesis is done by reducing the organification of iodine and decreasing the uptake. This effect is short lived and thyroid gland usually escapes from this phenomenon. Failure to escape from the detrimental effects of iodine excess results in hypothyroidism and goiter. The predisposing factors for iodine induced hypothyroidism are extremes of age, autoimmune thyroid disease and past history of treated Graves' disease. Previous reports suggest that modification of dietary constituents resulted in the normalization of (TSH) thyroid-stimulating hormone in children with subclinical hypothyroidism. [20]

Graves' disease and hyperthyroidism

Dietary alterations affect the thyroid function and may lead to hyperthyroidism due to excess iodine consumption. The other important management issue is consumption of iodine free diet prior to the nuclear imaging and thyroid radio ablation. Jod-Basedow phenomenon describes the occurrence of hyperthyroidism following the excess consumption of iodine. [21] This phenomenon is seen in patients of endemic goiter, people with multinodular goiter, Grave's disease and thyroid adenoma. This effect is typically opposite of Wolff-Chaikoff's effect and is not described in normal thyroid glands. The small increase of iodine intake in patients with a thyroid disorders with no pituitary control leads to Jod-Basedow phenomenon.

The management of differentiated thyroid carcinoma includes total thyroidectomy followed by ablation of thyroid remnant. Remnant ablation is preceded by thyroid hormone withdrawal or by therapy with recombinant human (TSH) thyroid-stimulating hormone prior to dosing the patient. Another important strategy to increase the radioiodide uptake is to create an iodine deplete stage by giving iodine free diet. The low plasma iodide concentration results in the increased expression of the sodium iodide symporter and increases the subsequent uptake of radioiodide by the thyroid gland. [22] The dietary measures to achieve a low iodine diet are given in [Table 1]. The beneficial effect of a low iodine diet is well established prior to iodine scan, but the same is not studied much before pertechnate scan. A study published recently suggests that low iodine diet for two weeks prior to technetium scan is beneficial in patients with multinodular goiter and seafood consumers. [23]
Table 1: How to take a low iodine diet

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Thyroid nodule

Thyroid nodule is a common disorder in the clinical practice and different nutritional and environmental factors are responsible for the etiopathogenesis of the nodule. Iodine deficiency and smoking increase the risk, whereas alcohol consumption and use of oral contraceptives are associated with reduced risk of goiter and the thyroid nodule. [24] Thiocyanate in the tobacco smoke inhibits iodine uptake by competitive inhibition and is the mediator of the goitrogenic effect.

Thyroid cancer

The incidence of thyroid cancer has been increasing over the past few decades for unexplained reasons. The alterations in dietary constituents and endocrine disruptors have been proposed as the contributing factors in the etiopathogenesis of thyroid cancer. Population studies exploring the link between dietary patterns and thyroid cancer revealed interesting findings. Dietary nitrite is an established risk factor for the thyroid cancer especially in males. Nitrate competitively inhibits iodide uptake, reduces the thyroid hormone synthesis leading to thyrotropinemia and thyroid hyperplasia with a potential to transform into thyroid cancer. [25] Nitrates also serve as the precursors for the formation of nitrosamines and nitrosamides which are potent carcinogenic substances. The highest concentration of nitrates is seen in leafy vegetables (spinach, lettuce) and beet-root. An increased risk of thyroid cancer was described with the consumption of cruciferous vegetables (thiocyanate consumption), butter, cheese, starchy food, pasta, meat and poultry products and a decreased risk with non cruciferous vegetables (especially carrots, green salad and citrus fruits), iodized salt, ham and fish. [26],[27],[28]

Miscellaneous topics

The topic of thyroid and diet is incomplete without mentioning about the soy proteins, perchlorate and the influence of maternal diet on the thyroid physiology. Numerous research papers have shown that the constituents of maternal diet during pregnancy have a profound influence on the fetal thyroid system leading to obesity during adulthood. Obesity and thyroid disease are interlinked with important physiological changes in the hypothalamo pituitary axis during weight gain. The topic of thyroid and obesity is the genesis behind a lot of myths associated with the thyroid diet. The print literature and internet has lead to lots of confusion in the minds of thyroid patients about their diet. The prevalent myths and relevant scientific facts are given in [Table 2].
Table 2: Myths and facts

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Soy protein and thyroid

Soy-containing foods and supplements are widely consumed for possible health benefits that include prevention of cancer, dyslipidemia, cardiovascular disease and osteoporosis. Genistein is the major soy isoflavone which has estrogenic and goitrogenic activity. [29] The antithyroid effects of genistein are exaggerated by the iodine deficiency. Genistein inhibits the activity of thyroid peroxidase in a dose dependent manner. The effects of soy isoflavones on the thyroid are dependent on the underlying iodine status and thyroid function. A metanalysis on the subject concludes that soy isoflavones have no adverse effects in euthyroid, iodine-replete individuals. There exists little evidence that soy foods may increase the thyroxine dose in hypothyroidism by inhibiting the absorption of levothyroxine. The hypothyroid adult patients need not avoid soy foods, but have to ensure adequate iodine content in their diet.

Perchlorate and thyroid

Perchlorate competitively inhibits the uptake of iodide into the thyroid gland, and affects the thyroid hormone synthesis. [30] The major contributors of perchlorate in the diet are vegetables, dairy products, drinking water and infant food products. The thyroid inhibitory actions of perchlorate were utilized by using this in iodine induced hyperthyroidism. In normal conditions, the presence of small perchlorate levels in water and food does not lead significant change in thyroid function due to the large iodine stores. Hence, no dietary modification is necessary for protection against the perchlorate induced thyroid dysfunction.

Maternal diet and fetal thyroid

Thyroid hormones also play an important role as a regulator of fetal development and energy expenditure. The amount and timing of thyroid hormone release are regulated through tight regulation of genes expressed within the hypothalamic-pituitary-thyroid axis. A fine balance is maintained between the production of T3 and T4 through tissue specific expression of the deiodinase, iodothyronine (DIO) genes. Maternal high fat diet leads to alterations in the hepatic histone code leading to transcriptional and epigenetic alterations of the fetal thyroid axis. Thus, in utero exposure to high fat diet may lead to obesity in later life by disturbing the fetal thyroid homeostasis. [31]

Obesity and thyroid

Thyroid hormone has a major influence on carbohydrate and lipid metabolism. Obesity is seen in hypofunctioning thyroid gland and is contributed by multiple factors like reduced metabolic rate, fluid retention and mucopolysaccharide deposition. [32] Leptin is the product of the ob gene, that regulates the food intake and body fat and previous reports gave conflicting results about the relation between leptin and thyroid hormones. [33]


  Conclusion Top


Dietary micronutrients play an important role in the synthesis of thyroid hormones. Iodine remains the cornerstone with increasing focus on other nutrients like selenium and zinc. Iodine consumption is a double edged sword with disorders emanating from both the deficiency and excess consumption. The best advice for all patients is to consume a healthy balanced diet, meet the daily iodine requirement and eliminate the most potent goitrogenic substances from the diet. There is a lot of hype behind the thyroid diet with limited scientific basis and it is advisable to follow the recommendations of the treating physician.

 
  References Top

1.
de Vijlder JJ. The iodine pathways within the thyroid gland: Pathological aspects. Ann Endocrinol (Paris) 2003;64:8-9.  Back to cited text no. 1
    
2.
Charlton K, Skeaff S. Iodine fortification: Why, when, what, how, and who? Curr Opin Clin Nutr Metab Care 2011;14:618-24.  Back to cited text no. 2
    
3.
Cléro É, Doyon F, Chungue V, Rachédi F, Boissin JL, Sebbag J, et al. Dietary patterns, goitrogenic food, and thyroid cancer: A case-control study in French Polynesia. Nutr Cancer 2012;64:929-36.  Back to cited text no. 3
    
4.
Das S, Bhansali A, Dutta P, Aggarwal A, Bansal MP, Garg D, et al. Persistence of goitre in the post-iodization phase: Micronutrient deficiency or thyroid autoimmunity? Indian J Med Res 2011;133:103-9.  Back to cited text no. 4
[PUBMED]  Medknow Journal  
5.
Hess SY. The impact of common micronutrient deficiencies on iodine and thyroid metabolism: The evidence from human studies. Best Pract Res Clin Endocrinol Metab 2010;24:117-32.  Back to cited text no. 5
    
6.
Braverman LE. The physiology and pathophysiology of iodine and the thyroid. Thyroid 2001;11:405.  Back to cited text no. 6
    
7.
Triggiani V, Tafaro E, Giagulli VA, Sabbà C, Resta F, Licchelli B, et al. Role of iodine, selenium and other micronutrients in thyroid function and disorders. Endocr Metab Immune Disord Drug Targets 2009;9:277-94.  Back to cited text no. 7
    
8.
Pearce EN, Andersson M, Zimmermann MB. Global iodine nutrition: Where do we stand in 2013? Thyroid 2013;23:523-8.  Back to cited text no. 8
    
9.
Zimmermann MB, Jooste PL, Pandav CS. Iodine-deficiency disorders. Lancet 2008;372:1251-62.  Back to cited text no. 9
    
10.
Zimmermann MB. Iodine deficiency. Endocr Rev 2009;30:376-408.  Back to cited text no. 10
    
11.
Zimmermann MB. Iodine deficiency and excess in children: Worldwide status in 2013. Endocr Pract 2013;19:839-46.  Back to cited text no. 11
    
12.
Srivastav A, Maisnam I, Dutta D, Ghosh S, Mukhopadhyay S, Chowdhury S. Cretinism revisited. Indian J Endocrinol Metab 2012;16(Suppl 2):S336-7.  Back to cited text no. 12
    
13.
Köhrle J. Pathophysiological relevance of selenium. J Endocrinol Invest 2013;36 (Suppl 10):1-7.  Back to cited text no. 13
    
14.
Köhrle J, Gärtner R. Selenium and thyroid. Best Pract Res Clin Endocrinol Metab 2009;23:815-27.  Back to cited text no. 14
    
15.
Zimmermann MB, Köhrle J. The impact of iron and selenium deficiencies on iodine and thyroid metabolism: Biochemistry and relevance to public health. Thyroid 2002;12:867-78.  Back to cited text no. 15
    
16.
Andersson M, Thankachan P, Muthayya S, Goud RB, Kurpad AV, Hurrell RF, et al. Dual fortification of salt with iodine and iron: A randomized, double-blind, controlled trial of micronized ferric pyrophosphate and encapsulated ferrous fumarate in southern India. Am J Clin Nutr 2008;88:1378-87.  Back to cited text no. 16
    
17.
Tonstad S, Nathan E, Oda K, Fraser G. Vegan diets and hypothyroidism. Nutrients 2013;5:4642-52.  Back to cited text no. 17
    
18.
Chandra AK, Mukhopadhyay S, Lahari D, Tripathy S. Goitrogenic content of Indian cyanogenic plant foods and their in vitro anti-thyroidal activity. Indian J Med Res 2004;119:180-5.  Back to cited text no. 18
    
19.
Leung AM, Braverman LE. Iodine-induced thyroid dysfunction. Curr Opin Endocrinol Diabetes Obes 2012;19:414-9.  Back to cited text no. 19
    
20.
Kuiper MW, van der Gaag EJ. Subclinical hypothyroidism in children can normalize after changes in dietary intake. Food Nutr Sci 2012;3:411-6.  Back to cited text no. 20
    
21.
Maberly GF, Corcoran JM, Eastman CJ. The effect of iodized oil on goitre size, thyroid function and the development of the Jod Basedow phenomenon. Clin Endocrinol (Oxf) 1982;17:253-9.  Back to cited text no. 21
    
22.
Ignacio Cuenca J, Ramón Rodríguez J, Guerrero R, Macías C, Jiménez L, Navarro E, et al. Utility of a low-iodide diet in (131) I whole body scanning of patients with differentiated thyroid cancer. Endocrinol Nutr 2008;55:117-22.  Back to cited text no. 22
    
23.
Javadi H, Neshandarasli I, Mogharrabi M, Jalallat S, Nabipour I, Assadi M. The effect of an iodine restricted including no sea foods diet, on technetium-99m thyroid scintigraphy: A neglected issue in nuclear medicine practice. Hell J Nucl Med 2012;15:40-2.  Back to cited text no. 23
    
24.
Knudsen N, Laurberg P, Perrild H, Bülow I, Ovesen L, Jørgensen T. Risk factors for goiter and thyroid nodules. Thyroid 2002;12:879-88.  Back to cited text no. 24
    
25.
Kilfoy BA, Zhang Y, Park Y, Holford TR, Schatzkin A, Hollenbeck A, et al. Dietary nitrate and nitrite and the risk of thyroid cancer in the NIH-AARP Diet and Health Study. Int J Cancer 2011;129:160-72.  Back to cited text no. 25
    
26.
Peterson E, De P, Nuttall R. BMI, diet and female reproductive factors as risks for thyroid cancer: A systematic review. PLoS One 2012;7:e29177.  Back to cited text no. 26
    
27.
Galanti MR, Hansson L, Bergström R, Wolk A, Hjartåker A, Lund E, 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;8:205-14.  Back to cited text no. 27
    
28.
Franceschi S, Levi F, Negri E, Fassina A, La Vecchia C. Diet and thyroid cancer: A pooled analysis of four European case-control studies. Int J Cancer 1991;48:395-8.  Back to cited text no. 28
    
29.
Messina M, Redmond G. Effects of soy protein and soybean isoflavones on thyroid function in healthy adults and hypothyroid patients: A review of the relevant literature. Thyroid 2006;16:249-58.  Back to cited text no. 29
    
30.
Leung AM, Pearce EN, Braverman LE. Perchlorate, iodine and the thyroid. Best Pract Res Clin Endocrinol Metab 2010;24:133-41.  Back to cited text no. 30
    
31.
Suter MA, Sangi-Haghpeykar H, Showalter L, Shope C, Hu M, Brown K, et al. Maternal high-fat diet modulates the fetal thyroid axis and thyroid gene expression in a nonhuman primate model. Mol Endocrinol 2012;26:2071-80.  Back to cited text no. 31
    
32.
Verma A, Jayaraman M, Kumar HK, Modi KD. Hypothyroidism and obesity. Cause or effect? Saudi Med J 2008;29:1135-8.  Back to cited text no. 32
    
33.
Duntas LH, Biondi B. The interconnections between obesity, thyroid function, and autoimmunity: The multifold role of leptin. Thyroid 2013;23:646-53.  Back to cited text no. 33
    


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