Department of Endocrinology, Aalborg Hospital, Aarhus University Hospital, DK - 9000 Aalborg, Denmark.
Best Pract Res Clin Endocrinol Metab. 2010 Feb;24(1):13-27. doi: 10.1016/j.beem.2009.08.013.
Depending on the availability of iodine, the thyroid gland is able to enhance or limit the use of iodine for thyroid hormone production. When compensation fails, as in severely iodine-deficient populations, hypothyroidism and developmental brain damage will be the dominating disorders. This is, out of all comparison, the most serious association between disease and the level of iodine intake in a population. In less severe iodine deficiency, the normal thyroid gland is able to adapt and keep thyroid hormone production within the normal range. However, the prolonged thyroid hyperactivity associated with such adaptation leads to thyroid growth, and during follicular cell proliferation there is a tendency to mutations leading to multifocal autonomous growth and function. In populations with mild and moderate iodine deficiency, such multifocal autonomous thyroid function is a common cause of hyperthyroidism in elderly people, and the prevalence of thyroid enlargement and nodularity is high. The average serum TSH tends to decrease with age in such populations caused by the high frequency of autonomous thyroid hormone production. On the other hand, epidemiological studies have shown that hypothyroidism is more prevalent in populations with a high iodine intake. Probably, this is also a complication to thyroid adaptation to iodine intake. Many thyroid processes are inhibited when iodine intake becomes high, and the frequency of apoptosis of follicular cells becomes higher. Abnormal inhibition of thyroid function by high levels of iodine is especially common in people affected by thyroid autoimmunity (Hashimoto's thyroiditis). In populations with high iodine intake, the average serum thyroid-stimulating hormone (TSH) tends to increase with age. This phenomenon is especially pronounced in Caucasian populations with a genetically determined high tendency to thyroid autoimmunity. A small tendency to higher serum TSH may be observed already when iodine intake is brought from mildly deficient to adequate, but there is at present no evidence that slightly elevated serum TSH in elderly people leads to an increase in morbidity and mortality.
Even minor differences in iodine intake between populations are associated with differences in the occurrence of thyroid disorders. Both iodine intake levels below and above the recommended interval are associated with an increase in the risk of disease in the population. Optimally, iodine intake of a population should be kept within a relatively narrow interval where iodine deficiency disorders are prevented, but not higher. Monitoring and adjusting of iodine intake in a population is an important part of preventive medicine.
甲状腺能够根据碘的供应情况增强或限制甲状腺激素的生成。当补偿失败时,比如在严重缺碘人群中,就会出现甲状腺功能减退和发育性脑损伤。这是所有人群碘摄入量与疾病之间最严重的关联。在碘缺乏不太严重的情况下,正常的甲状腺能够适应并将甲状腺激素的生成维持在正常范围内。然而,与这种适应相关的甲状腺长期亢进会导致甲状腺生长,在滤泡细胞增殖过程中,存在向多灶性自主性生长和功能转化的趋势。在碘轻度和中度缺乏的人群中,这种多灶性自主性甲状腺功能是老年人甲状腺功能亢进的常见原因,甲状腺肿大和结节的患病率很高。由于自主甲状腺激素生成的高频率,此类人群的平均血清 TSH 随着年龄的增长而趋于降低。另一方面,流行病学研究表明,高碘摄入人群中甲状腺功能减退更为常见。这可能也是甲状腺适应碘摄入的一种并发症。当碘摄入增加时,许多甲状腺过程受到抑制,滤泡细胞的凋亡频率更高。高碘水平对甲状腺功能的异常抑制在受甲状腺自身免疫(桥本甲状腺炎)影响的人群中尤为常见。在碘摄入量高的人群中,平均血清促甲状腺激素(TSH)随着年龄的增长而增加。这种现象在具有遗传决定的高甲状腺自身免疫倾向的白种人群中尤为明显。当碘摄入量从轻度缺乏增加到足够时,可能会观察到稍高的血清 TSH 趋势,但目前尚无证据表明老年人的血清 TSH 轻度升高会导致发病率和死亡率增加。
即使人群之间的碘摄入量存在微小差异,也与甲状腺疾病的发生存在差异相关。碘摄入量低于和高于推荐区间都会增加人群的患病风险。最理想的情况是,将人群的碘摄入量保持在一个相对狭窄的区间内,以预防碘缺乏症,但不要过高。监测和调整人群的碘摄入量是预防医学的重要组成部分。