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Quantitative Biology > Tissues and Organs

arXiv:2503.02981 (q-bio)
[Submitted on 4 Mar 2025 ]

Title: Modeling Iodine Deficiency

Title: 碘缺乏建模

Authors:Paul Fong, Albert Li, Zoe Meadows, Rati Pillai, Chelsea Proutt, Alex Schneider
Abstract: This paper presents a four-unit, four-component mathematical model of iodine metabolism and its impact on thyroid hormone levels in the body. We focus on the relationships between iodine (I-), triiodothyronine (T3), thyroxine (T4), and thyroid-stimulating hormone (TSH) through the mixer, thyroid, sensor (pituitary gland), and metabolism. Iodine plays a fundamental role in maintaining metabolic homeostasis, as it is essential for the synthesis of T3 and T4, which regulate weight, energy, and other physiological functions. Iodine deficiency, which is one of the most common nutrient deficiencies in the world, can lead to hypothyroidism, a condition characterized by fatigue, weight gain, and cognitive impairments [1]. Our model tracks the movement of iodine through dietary intake, thyroid absorption, hormone synthesis, feedback regulation via TSH, and deiodization in metabolism. By evaluating different forms of the accounting equation governing these processes, we have concluded three key results. 1) Iodide availability directly impacts levels of T3 and T4 production, with both component flow rates declining at day 70 in a mildly diseased state, and day 60 in a severely diseased state. 2) TSH is an early diagnostic indicator of thyroid issues, with TSH levels rising to magnitudes of 25x in just ten days, nearly six times quicker than other biological indicators. 3) There is a 5 day difference in iodine storage depletion between mild and severe iodide deficiency. Understanding these results quantitatively provides insights into thyroid disorders and informs strategies for managing iodine deficiency on both individual and public health levels.
Abstract: 本文提出了一种四单元、四组分的碘代谢数学模型,以及其对体内甲状腺激素水平的影响。 我们通过混合器、甲状腺、传感器(垂体腺)和代谢过程,关注碘(I-)、三碘甲状腺原氨酸(T3)、甲状腺素(T4)和促甲状腺激素(TSH)之间的关系。 碘在维持代谢稳态中起着基础作用,因为它对于合成调节体重、能量和其他生理功能的T3和T4是必不可少的。 碘缺乏是世界上最常见的营养缺乏之一,可能导致甲状腺功能减退症,其特征是疲劳、体重增加和认知障碍[1]。 我们的模型追踪碘通过饮食摄入、甲状腺吸收、激素合成、通过TSH的反馈调节以及代谢中的脱碘作用的运动过程。 通过评估控制这些过程的会计方程的不同形式,我们得出了三个关键结果。 1)碘化物的可用性直接影响T3和T4的生成水平,在轻度疾病状态下,第70天两种组分的流量都会下降,而在严重疾病状态下,第60天就会下降。 2)TSH是甲状腺问题的早期诊断指标,TSH水平在短短十天内上升到25倍,比其他生物指标快近六倍。 3)轻度和重度碘化物缺乏之间存在5天的碘储存耗尽差异。 定量理解这些结果为甲状腺疾病提供了见解,并为在个人和公共卫生层面管理碘缺乏症提供了依据。
Comments: 46 pages, 8 figures,
Subjects: Tissues and Organs (q-bio.TO) ; Biomolecules (q-bio.BM)
Cite as: arXiv:2503.02981 [q-bio.TO]
  (or arXiv:2503.02981v1 [q-bio.TO] for this version)
  https://doi.org/10.48550/arXiv.2503.02981
arXiv-issued DOI via DataCite

Submission history

From: Alexander Schneider [view email]
[v1] Tue, 4 Mar 2025 20:14:35 UTC (1,950 KB)
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