THE IMPORTANCE OF IODINE FOR THE HUMAN ORGANISM

Аннотация

Iodine plays a crucial role in human physiology as an essential component of thyroid hormones. This review examines iodine's biological significance, consequences of deficiency, and preventive measures. Current data indicates that iodine deficiency affects nearly 1.9 billion people worldwide, particularly impacting cognitive development in children and pregnant women. The paper analyzes thyroid dysfunction mechanisms (hypothyroidism, hyperthyroidism) and their clinical manifestations. We discuss diagnostic approaches and public health strategies for iodine deficiency disorders (IDDs), emphasizing the importance of universal salt iodization programs. Recent research on iodine's extra- thyroidal functions and optimal supplementationguidelines are also presented. Keywords: iodinedeficiency, hypothyroidism, hyperthyroidism, thyroid dysfunction, goiter 1.Introduction Iodine is a vital micronutrient required for thyroid hormone synthesis, with recommended daily intake ranging from 90μg (infants) to 200μg (pregnant women) [WHO, 2023]. Approximately 31% of the global population remains at risk of iodine deficiency disorders (IDDs), particularly in mountainous regions and areas with lowsoiliodinecontent [1]. The thyroid gland utilizes iodine toproduce thyroxine (T4) and triiodothyronine (T3), which regulate:  Basal metabolicrate  Neurocognitivedevelopment  Cardiovascular function  Reproductivehealth Thispaper systematically reviews: 1. Iodine's physiological roles 2. Pathogenesis ofiodinedeficiency disorders 3. Clinical management strategies 4. Current prevention programs 98,7:ROTCAFTCAPMI.SECNEICSLACIDEM ,5202 ,lirpA,5emuloV gro.srehsilbupcimedaca.www 2.Materials andMethods We analyzed 48 peer-reviewed studies (2018-2023) from PubMed, Scopus, and WHO databases using keywords: "iodine deficiency", "thyroid pathophysiology", and "iodine prophylaxis". 3.Results andDiscussion 3.1EpidemiologicalData  Global prevalence: 1.9billionat risk, including350million Europeans [2]  Highest risk groups: Pregnant women (increased fetal requirements) o Children(neurodevelopmental vulnerability) o 3.2PathophysiologicalMechanisms IodineDeficiency Consequences: Severity Clinical Manifestations Mild Fatigue, weight gain ModerateGoiter, cognitiveimpairment Severe Cretinism,stillbirth ThyroidDysfunctionTypes: 1. Hypothyroidism:Reduced hormone production Symptoms:Bradycardia, cold intolerance o 2. Hyperthyroidism: Excessivehormonesecretion Symptoms:Tachycardia, weight loss o 3.3DiagnosticApproaches  Laboratory tests:TSH, free T4, urinary iodine  Imaging: Thyroid ultrasound, scintigraphy 3.4Prevention Strategies  Universal salt iodization (USI) programs  Dietary sources: Seafood (150-1000μg/100g) o Iodizedsalt (20-40μg/g) o Dairy products (30-50μg/100ml) o The present review synthesizes current evidence on iodine's pivotal role in human physiology and the far-reaching consequences of its deficiency. Our analysis reveals several critical findings that warrant further examination. 98,7:ROTCAFTCAPMI.SECNEICSLACIDEM ,5202 ,lirpA,5emuloV gro.srehsilbupcimedaca.www 5.1GlobalHealth Implications The persistent burden of iodine deficiency disorders (IDDs) among 1.9 billion individuals underscores a significant public health challenge. While universal salt iodization (USI) programs have reduced goiter prevalence by 40% in endemic regions since 1990 [Zimmermann, 2021], emerging data suggests:  Geographic disparities: Mountainous and inland populations show 3× higher deficiency rates than coastal communities [WHO, 2023]  Vulnerability paradox: Despite global progress, pregnant women in Europe exhibit rising deficiency rates (from 15% to 21% during 2015-2022) due to reduced salt consumptiontrends [2] 5.2PathophysiologicalInsights Ourexaminationof thyroid dysfunction mechanisms reveals two key phenomena: 1. The J-shaped risk curve: Both deficiency ( 500 μg/day) iodineintake correlatewith thyroid dysfunction [Leung, 2023] 2. Selenium interplay: The selenoenzyme deiodinase's role explains why concurrent selenium deficiency exacerbates hypothyroidism iniodine-deficient populations[3] Notably, thetransitionfrom subclinical to overt hypothyroidism follows adistinct pattern:  Stage1: Increased TSH with normalT4 (compensated)  Stage 2: Elevated TSH with low T4 (decompensated) This progression highlights the importance of early detection through neonatal screening programs, which prevent 70% ofintellectual disabilitycases inendemic regions [1]. 5.3DiagnosticandTherapeutic Challenges Current approaches present several limitations: Method SensitivitySpecificity Urinary iodine 82% 75% Thyroid ultrasound91% 88% TSHtesting 95% 89% Key unresolved issues include:  "Iodine paradox": Some populations develop autoimmune thyroiditis post- iodization  Supplementation timing: Optimal iodine doses for pregnant women remain debated (150-250 μg/day) 5.4Prevention Strategies Re-evaluation 98,7:ROTCAFTCAPMI.SECNEICSLACIDEM ,5202 ,lirpA,5em