SUBSCRIBE

甲状腺健康jiazhuangxianjiankang

甲状腺肿的营养支持策略:碘、锰、维生素

时间:2021-04-12 16:46 阅读:258 来源:朴诺健康研究院

同义索引:碘缺乏性甲状腺功能减退症

  1. 简介

  2. 一览表 

  3. 症状

  4. 治疗 

  5. 饮食习惯的改变 

  6. 营养补充剂

  7. 参考文献


甲状腺肿是指甲状腺体积增大,常常可看到患者颈部前方明显肿大。


甲状腺体积增大的原因很多,包括碘缺乏,机体利用碘能力下降,或多种甲状腺机能紊乱,另外,还可能包括感染、肿瘤以及自身免疫性疾病。一些环境污染物,重金属毒物,以及某些药物也可以导致甲状腺肿[1,2,3]。碘缺乏和机体利用碘能力下降都会导致甲状腺无法产生甲状腺激素,而该激素是一种协助机体调节代谢率的激素。这种状况称为“甲状腺机能减退”,症状包括疲乏,体重增加,女性月经增多,皮肤毛发干燥,以及甲状腺肿大。


碘缺乏性甲状腺肿在土壤和食物中缺乏碘元素的地区比较常见。学龄前儿童,青春期少女,怀孕妇女和老人最容易患甲状腺肿和其它碘缺乏相关的疾病[4]。碘供应不足地区除了甲状腺肿的高发病率外,出生缺陷以及身心发育迟缓的发病率也高[5]。虽然在整个世界范围内,碘缺乏是甲状腺肿的头号病因,在发达国家却很少发生。正因如此,在发达国家中一旦发现甲状腺肿,必须由卫生保健人员进行评估,在治疗之前明确病因。


甲状腺肿的辅助疗法


分类营养补充剂草药
首选/
次选

锰 (如有缺乏,应给予补充)

维生素A

维生素E

锌 (如有缺乏,应给予补充)

/
首选 有可靠和相对一致的科研数据证明其对健康有显著改善。

次选 各有关科研结果相互矛盾、证据不充分或仅能初步表明其可改善健康状况或效果甚微。

其它 对草药来说,仅有传统用法可支持其应用,但尚无或仅有少量科学证据可证明其疗效。对营养补充剂来说,无科学证据支持和/或效果甚微。


甲状腺肿的症状


甲状腺肿的患者在颈前部有一明显的柔软肿物。



医药治疗


甲状腺激素替代疗法,如左旋甲状腺素(Synthroid, Levoxyl)和干甲状腺片(Armour Thyroid)是针对甲状腺肿患者的处方药。


其它的疗法包括食盐加碘和避免致甲状腺肿的食物,这类食物包括卷心菜,芽甘蓝和大豆等等。当出于美观考虑,或肿大的甲状腺引起对呼吸和吞咽的压迫症状时,可以考虑手术摘除或放射性碘疗法。


可能有益的饮食习惯


在治疗碘缺乏性甲状腺功能减退症和预防甲状腺肿的问题上,饮食方面最重要的就是保证足够量碘的摄入。碘可以在海源性的天然食物中找到,例如鱼类和海产品,海藻和海菜;此外,水土中富含碘地区的动物和植物食品中也有比较丰富的碘[6.7]。在发达国家,自从1920年以来,商业性食用盐就被强制加碘以防止碘缺乏[8]。在每克加碘盐中大概含有100微克的碘。这种加碘盐可以直接使用,并加入到动物饲料和食品加工过程中,以便达到对于青少年和成人的150微克的“建议饮食摄取量”(Recommended Dietary Allowance,RDA),以及对于孕期和哺乳期妇女的200微克的“建议饮食摄取量”[9]。加碘盐的效果被证明是如此的好,以至于它被推荐为全球消除碘缺乏的干预措施[10,11]。碘化油,每年一次的注射或口服,也被有效的用于治疗碘缺乏性甲状腺肿[12,13]


尽管碘缺乏与甲状腺肿在今天的发达国家已经相当罕见,但新近的研究表明美国人每日的碘摄取量已经低于了“建议饮食摄取量”[14]。长时间的饮食中过度的碘摄入(每天1000-2000微克),尽管不如碘缺乏常见,也发生在进食大量海藻和其它海菜的人群中,也会导致甲状腺肿[15,16]


一些平时常见的食物已经被证实可以干扰甲状腺对碘的利用,降低甲状腺激素的产生,并导致甲状腺肿。这些食物,被称为致甲状腺肿原,包括芸苔科蔬菜,如花椰菜、卷心菜、羽衣甘蓝,此外还有芥菜[17]、黍[18]、大豆[19]、松果[20]和动物饲料中采用的谷物粗粉[21,22]。这些食物对于摄碘正常的人群,摄取适量还是很安全的[23]。但低碘摄取合并高的致甲状腺肿食物的摄取,则会增加甲状腺肿的发病率[24,25]


营养素的缺乏,包括锌[26],锰[27]和维生素A[28,29],以及严重的蛋白质营养失调[30]也会导致机体使用碘能力的下降和甲状腺肿的发生[31,32]。在机体摄碘充足的情况下,上述营养物质的缺乏不太容易引起甲状腺肿[33,34];但是,当碘的摄入不足,及时是轻度的不足,上述因素也会对甲状腺功能产生负面影响[35,36]。高浓度的矿物质,例如钙和镁,以及某些饮用水中的细菌,也被证实是致甲状腺肿的[37,38]。因此,合适的营养和卫生的饮用水供应对于预防和治疗甲状腺肿是非常重要的。


可能有益的营养补充剂



碘的补充能够有效的治疗碘缺乏性甲状腺功能减低症,当病因没有营养不良以及环境或食物中的致甲状腺肿原等复杂因素掺杂时,补碘可以很好的抑制甲状腺肿的进展[39,40]。对于甲状腺肿的早期阶段,补碘可以有助于肿块的缩小;但对于晚期阶段,则没有效果[41]。长期的每日摄入2000-6000微克碘可以对甲状腺产生毒性,成为导致甲状腺肿的又一病因[42,43]


维生素A


患有甲状腺肿的人群,其血浆中的维生素A含量低于健康人群[44,45]。对于维生素E,也发现了同样的现象[46]。动物实验的结果表明,在缺碘的情况下,维生素C,维生素E和β-胡萝卜素的复合制剂可以预防甲状腺肿的形成(尽管甲状腺功能减低并没有被改善),仅使用维生素E可以达到类似的效果[47]。至今尚没有类似研究针对人类进行,故尚不清楚这些益处对于人类是否适用。


锌、锰、硒


当碘缺乏发生时,其它营养物质的水平在甲状腺肿的发展中也变得重要起来。锌[48]和锰[49]的缺乏对于碘缺乏性甲状腺肿都有促进作用;然而,一项动物实验表明,过量的锰同样会导致甲状腺肿[50]。还有研究表明硒的缺乏可能对甲状腺肿的发生起一定作用[51]。然而,当对碘、硒双缺乏的患者使用硒剂时,甲状腺机能减低的现象反而恶化,可能硒的缺乏可能对碘缺乏有一定的保护作用[52,53]。一项针对不缺乏硒,却有轻度的低碘的女性的研究发现,每天补充100微克的硒,对于甲状腺机能没有影响[54]。作者总结说硒剂似乎对于仅缺碘,不缺硒的患者安全;而对于硒、碘双缺乏的人来说则不然。在硒、碘双缺乏的情况时,碘的补充被证明是最有效的[55]。至今还没有研究来评估锌和锰的补充对于预防甲状腺肿的作用。


有无副作用及药物之间相互作用?

请参考各种草药的副作用及相互作用。

 

参考文献


1. Prescott E, Netterstrom B, Faber J, et al. Effect of occupational exposure to cobalt blue dyes on the thyroid volume and function of female plate painters. Scand J Work Environ Health 1992;18:101–4.

2. Gaitan E. Goitrogens. Baillieres Clin Endocrinol Metab 1988;2:683–702 [review].

3. Gaitan E. Goitrogens in food and water. Annu Rev Nutr 1990;10:21–39 [review].

4. Ingenbleek Y, De Visscher M. Hormonal and nutritional status: critical conditions for endemic goiter epidemiology? Metabolism 1979;28:9–19 [review].

5. Lamberg BA. Endemic goitre—iodine deficiency disorders. Ann Med 1991;23:367–72 [review].

6. Lamberg BA. Iodine deficiency disorders and endemic goitre. Eur J Clin Nutr 1993;47:1–8 [review].

7. Koutras DA. Iodine metabolism in endemic goitre. Ann Clin Res 1972;4:55–63 [review].

8. Lee K, Bradley R, Dwyer J, Lee S. Too much versus too little: The implications of current iodine intake in the United States. Nutr Rev 1999;57:177–81 [review].

9. Lee K, Bradley R, Dwyer J, Lee S. Too much versus too little: The implications of current iodine intake in the United States. Nutr Rev 1999;57:177–81 [review].

10. Lamberg BA. Endemic goitre—iodine deficiency disorders. Ann Med 1991;23:367–72 [review].

11. Dunn JT. Seven deadly sins in confronting endemic iodine deficiency, and how to avoid them. J Clin Endocrinol Metab 1996;81:1332–5 [review].

12. Ingenbleek Y, Jung L, Ferard G. Brassiodol, a new iodised oil for goitrous patients. Coll Antropol 1998;22:51–62.

13. Untoro J, Schultink W, Gross R, et al. Efficacy of different types of iodised oil. Lancet 1998;351:752–3.

14. Lee K, Bradley R, Dwyer J, Lee S. Too much versus too little: The implications of current iodine intake in the United States. Nutr Rev 1999;57:177–81 [review].

15. Franceschi S, Talamini R, Fassina A, Bidoli E. Diet and epithelial cancer of the thyroid gland. Tumori 1990;76:331–8 [review].

16. Wilson JD, Foster DW, Kronenberg HM, Larsen PR. Williams Textbook of Endocrinology, 9th edition. Philadelphia: WB Saunders Co, 1998, 469.

17. Stoewsand GS. Bioactive organosulfur phytochemicals in Brassica oleracea vegetables—a review. Food Chem Toxicol 1995;33:537–43 [review].

18. Sartelet H, Serghat S, Lobstein A, et al. Flavonoids extracted from fonio millet (Digitaria exilis) reveal potent antithyroid properties. Nutrition 1996;12:100–6.

19. Divi RL, Chang HC, Doerge DR. Anti-thyroid isoflavones from soybean: isolation, characterization and mechanisms of action. Biochem Pharmacol 1997;54:1087–96.

20. Gaitan E. Goitrogens in food and water. Annu Rev Nutr 1990;10:21–39 [review].

21. Mawson R, Heaney RK, Zdunczyk Z, Kozlowska H. Rapeseed meal-glucosinolates and their antinutritional effects. Part 4. Goitrogenicity and internal organs abnormalities in animals. Nahrung 1994;38:178–91.

22. Bell JM. Nutrients and toxicants in rapeseed meal: a review. J Anim Sci 1984;58:996–1010 [review].

23. Gaitan E. Goitrogens. Baillieres Clin Endocrinol Metab 1988;2:683–702 [review].

24. Gaitan E. Goitrogens. Baillieres Clin Endocrinol Metab 1988;2:683–702 [review].

25. Gaitan E. Goitrogens in food and water. Annu Rev Nutr 1990;10:21–39 [review].

26. Ozata M, Salk M, Aydin A, et al. Iodine and zinc, but not selenium and copper, deficiency exists in a male Turkish population with endemic goiter. Biol Trace Elem Res 1999;69:211–6.

27. Kawada J, Nishida M, Yoshimura Y, Yamashita K. Manganese ion as a goitrogen in the female mouse. Endocrinol Jpn 1985;32:635–43.

28. Ingenbleek Y, Luypaert B, De Nayer P. Nutritional status and endemic goitre. Lancet 1980;1:388–91.

29. Osman AK, Fatah AA. Factors other than iodine deficiency contributing to the endemicity of goitre in Darfur Province (Sudan). J Hum Nutr 1981;35:302–9.

30. Ingenbleek Y, Luypaert B, De Nayer P. Nutritional status and endemic goitre. Lancet 1980;1:388–91.

31. Osman AK, Fatah AA. Factors other than iodine deficiency contributing to the endemicity of goitre in Darfur Province (Sudan). J Hum Nutr 1981;35:302–9.

32. Gaur DR, Sood AK, Gupta VP. Goitre in school girls of the Mewat area of Haryana. Indian Pediatr 1989;26:223–7.

33. Gaitan E. Goitrogens. Baillieres Clin Endocrinol Metab 1988;2:683–702 [review].

34. Lamberg BA. Endemic goitre--iodine deficiency disorders. Ann Med 1991;23:367–72 [review].

35. Centanni M, Maiani G, Vermiglio F, et al. Combined impairment of nutritional parameters and thyroid homeostasis in mildly iodine-deficient children. Thyroid 1998;8:155–9.

36. Filteau SM, Sullivan KR, Anwar US, et al. Iodine deficiency alone cannot account for goitre prevalence among pregnant women in Modhupur, Bangladesh. Eur J Clin Nutr 1994;48:293–302.

37. Gaur DR, Sood AK, Gupta VP. Goiter in school children of the Mewat area of Haryana. Indian Pediatr 1989;26:223–7.

38. Gaitan E. Goitrogens in food and water. Annu Rev Nutr 1990;10:21–39 [review].

39. Koutras DA. Iodine metabolism in endemic goitre. Ann Clin Res 1972;4:55–63 [review].

40. Lee K, Bradley R, Dwyer J, Lee S. Too much versus too little: The implications of current iodine intake in the United States. Nutr Rev 1999;57:177–81 [review].

41. Cotran RS, Kumar V, Robbins SL. Robbins Pathologic Basis of Disease, 4th edition. Philadelphia: WB Saunders Co, 1989, 1227–8.

42. Gaitan E. Goitrogens in food and water. Annu Rev Nutr 1990;10:21–39 [review].

43. Wilson JD, Foster DW, Kronenberg HM, Larsen PR. Williams Textbook of Endocrinology, 9th edition. Philadelphia: WB Saunders Co, 1998, 469.

44. Keyvani F, Yassai M, Kimiagar M. Vitamin A status and endemic goiter. Int J Vitam Nutr Res 1988;58:155–60.

45. Mesaros-Kanjski E, Kontosic I, Kusic Z, et al. Endemic goitre and plasmatic levels of vitamins A and E in the school-children on the island of Krk, Croatia. Coll Antropol 1999;23:729–36.

46. Mesaros-Kanjski E, Kontosic I, Kusic Z, et al. Endemic goitre and plasmatic levels of vitamins A and E in the school-children on the island of Krk, Croatia. Coll Antropol 1999;23:729–36.

47. Mutaku JF, Many MC, Colin I, et al. Antigoitrogenic effect of combined supplementation with dl-alpha-tocopherol, ascorbic acid and beta-carotene and of dl-alpha-tocopherol alone in the rat. J Endocrinol 1998;156:551–61.

48. Ozata M, Salk M, Aydin A, et al. Iodine and zinc, but not selenium and copper, deficiency exists in a male Turkish population with endemic goiter. Biol Trace Elem Res 1999;69:211–6.

49. Kawada J, Nishida M, Yoshimura Y, Yamashita K. Manganese ion as a goitrogen in the female mouse. Endocrinol Jpn 1985;32:635–43.

50. Kawada J, Nishida M, Yoshimura Y, Yamashita K. Manganese ion as a goitrogen in the female mouse. Endocrinol Jpn 1985;32:635–43.

51. Untoro J, Ruz M, Gross R. Low environmental selenium availability as an additional determinant for goiter in East Java, Indonesia? Biol Trace Elem Res 1999;70:127–36.

52. Corvilain B, Contempre B, Longombe AO, et al. Selenium and the thyroid: how the relationship was established. Am J Clin Nutr 1993;57:244S–248S [review].

53. Vanderpas JB, Contempre B, Duale NL, et al. Selenium deficiency mitigates hypothyroxinemia in iodine-deficient subjects. Am J Clin Nutr 1993 Feb;57(2 Suppl):271S–275S [review].

54. Roti E, Minelli R, Gardini E, et al. Selenium administration does not cause thyroid insufficiency in subjects with mild iodine deficiency and sufficient selenium intake. J Endocrinol Invest 1993;7:481–4.

55. Zimmermann MB, Adou P, Torresani T, et al. Effect of oral iodized oil on thyroid size and thyroid hormone metabolism in children with concurrent selenium and iodine deficiency. Eur J Clin Nutr 2000;3:209–13.