Popova Elizaveta V, Tinkov Alexey A, Ajsuvakova Olga P, Skalnaya Margarita G, Skalny Anatoly V
Orenburg State Medical University, Orenburg, Russia; St Joseph University in Tanzania, St Joseph College of Health Sciences, Dar es salaam, Tanzania.
Orenburg State Medical University, Orenburg, Russia; Yaroslavl State University, Yaroslavl, Russia; RUDN University, Moscow, Russia.
Med Hypotheses. 2017 Jul;104:63-67. doi: 10.1016/j.mehy.2017.05.024. Epub 2017 May 26.
The iodine deficiency disorders (IDD) include a variety of disturbances such as decreased fertility, increased perinatal and infant mortality, impaired physical and intellectual development, mental retardation, cretinism, hypothyroidism, and endemic goiter (EG). The occurrence of the latter is determined by interplay between genetic and environmental factors. The major environmental factor is iodine status that is required for normal thyroid hormone synthesis. However, other factors like intake of micronutrients and goiterogens also have a significant impact. Essential and toxic trace elements both play a significant role in thyroid physiology. We hypothesize that in terms of overexposure boron may serve as a potential goiterogen. In particular, it is proposed that boron overload may impair thyroid physiology ultimately leading to goiter formation. Certain studies provide evidential support of the hypothesis. In particular, it has been demonstrated that serum and urinary B levels are characterized by a negative association with thyroid hormone levels in exposed subjects. Single indications on the potential efficiency of B in hypothyroidism also exist. Moreover, the levels of B were found to be interrelated with thyroid volume in children environmentally exposed to boron. Experimental studies also demonstrated a significant impact of boron on thyroid structure and hormone levels. Finally, the high rate of B cumulation in thyroid may also indicate that thyroid is the target for B activity. Chemical properties of iodine and boron also provide a background for certain competition. However, it is questionable whether these interactions may occur in the biological systems. Further clinical and experimental studies are required to support the hypothesis of the involvement of boron overexposure in goiter formation. If such association will be confirmed and the potential mechanisms elucidated, it will help to regulate the incidence of hypothyroidism and goiter in endemic regions with high boron levels in soil and water.
碘缺乏病（IDD）包括多种病症，如生育能力下降、围产期和婴儿死亡率增加、身体和智力发育受损、智力迟钝、呆小症、甲状腺功能减退以及地方性甲状腺肿（EG）。后者的发生取决于遗传和环境因素之间的相互作用。主要的环境因素是正常甲状腺激素合成所需的碘状态。然而，其他因素如微量营养素和致甲状腺肿物质的摄入也有重大影响。必需微量元素和有毒微量元素在甲状腺生理学中都起着重要作用。我们假设，就过度暴露而言，硼可能是一种潜在的致甲状腺肿物质。特别是，有人提出硼过载可能损害甲状腺生理学，最终导致甲状腺肿形成。某些研究为这一假设提供了证据支持。特别是，已经证明，在接触者中，血清和尿液中的硼水平与甲状腺激素水平呈负相关。也有关于硼在甲状腺功能减退症中潜在疗效的单一迹象。此外，在环境中接触硼的儿童中，发现硼水平与甲状腺体积相关。实验研究也证明了硼对甲状腺结构和激素水平有重大影响。最后，硼在甲状腺中的高累积率也可能表明甲状腺是硼作用的靶器官。碘和硼的化学性质也为某些竞争提供了背景。然而，这些相互作用是否会在生物系统中发生仍值得怀疑。需要进一步的临床和实验研究来支持硼过度暴露参与甲状腺肿形成这一假设。如果这种关联得到证实并阐明潜在机制，将有助于调节土壤和水中硼含量高的地方性地区甲状腺功能减退症和甲状腺肿的发病率。
