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Iodine in human health Iodine Deficiency Disorderes.

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Presentation on theme: "Iodine in human health Iodine Deficiency Disorderes."— Presentation transcript:

1 Iodine in human health Iodine Deficiency Disorderes

2 ● Iodine is a chemical element ( as are Oxygen,Hydrogen, Iron ) occurs in a variety of chemical forms ● Iodine is an essential trace element for the human ● Iodine is an essential part of the chemical structure of thyroid hormones Total quantity present in body is (15-20 mg) Mostly in thyroid gland

3 Iodine  A non-metallic trace element, is required by humans for the synthesis of thyroid hormones thyroidhormonesthyroidhormones  Iodine deficiency is an important health problem throughout much of the world  Because iodine deficiency results in increased iodine trapping by the thyroid, iodine deficient individuals of all ages are more susceptible to radiation-induced thyroid cancer

4 Deficiency  According to the World Health Organization (WHO), iodine deficiency disorders (IDD) affect 740 million people throughout the world, and nearly 50 million people suffer from some degree of IDD-related brain damage  mental retardation, hypothyroidism, goiter, and varying degrees of other growth and developmental abnormalities hypothyroidismgoiterhypothyroidismgoiter

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6  Seawater contains 50 ppm (parts per million) iodine which means that there are approximately 76 billion pounds of iodine in the world’s oceans.  Iodine was first discovered in seaweed.  Dried seaweeds, particularly those of the Liminaria family, contain as much as 0.45% iodine. 6/4/20166

7  Seaweed was a major source of iodine before 1959.  Seaweed is a significant source for iodine in the diets of many people around the world.  Production from caliche is presently the most economical of the options listed here 6/4/20167

8  Daily adult requirements, currently recommended at 150 µg/day, could be covered by very small quantities of seaweed.  Just one gram of dried brown algae provides from 500-8,000 µg of iodine  Even the green and red algae (such as the purple nori that is used in Japanese cuisine) provides 100-300 µg in a single gram. 6/4/20168

9 Iodine absorption  Oral. Iodine appears to be inactivated by combination with gastrointestinal contents. Absorption is poor due to rapid conversion of iodine to iodide. (Reynolds, 1989; Gilman et al., 1990).  "Inhalation. Iodine is absorbed from the lungs, converted to iodide in the body, (ILO 1971). Pulmonary absorption of vapour may result in systemic poisoning (Gosselin et al., 1984).  6/4/20169

10 Absorption……. "Dermal. Only very small quantities of iodine are absorbed through an intact skin, (Reynolds, 1989).  Iodine can be absorbed by wounds and abrasions.  Enhanced absorption occurs through denuded skin, decubitus ulcers, mucosal surfaces with high absorptive capacity, or large areas of intact skin, (Dela Cruz et al., 1987; Vorherr et al., 1989; Prager & Gardner 1979; Cosman et al., 1988).  Enhanced absorption occurs through denuded skin, decubitus ulcers, mucosal surfaces with high absorptive capacity, or large areas of intact skin, (Dela Cruz et al., 1987; Vorherr et al., 1989; Prager & Gardner 1979; Cosman et al., 1988).  "Eye. Iodine can be absorbed when applied on the eye, (Geisthoevel, 1984).  "Eye. Iodine can be absorbed when applied on the eye, (Geisthoevel, 1984). 6/4/201610

11 Iodine transport  Active I - accumulation in the thyroid is mediated by the Na + / I - symporter (NIS), a plasma membrane glycoprotein  Using as its driving force the Na+ gradient generated by the Na + _-K + _-ATPase, NIS couples the inward movement of Na + in favor of its concentration gradient to the inward movement of I - against its electrochemical gradient.  Characteristic hallmarks of NIS are its Na dependence 6/4/201611

12  NIS mediates I uptake in several tissues besides the thyroid, including :  Lactating mammary gland,  Gastric mucosa,  & salivary glands  It appears that Na + / I - symporter is present in GI tract small intestine) 6/4/201612

13 Pyramidal lobe 6/4/201613

14 Thyroid Hormones Contain 3-4 Atoms of Iodine

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16 Role of Iodine  Iodine is needed for the synthesis of thyroid hormones.  Thyroid hormone: Metabolic Thermogenic Carbohydrate metabolism Protein metabolism Fat metabolism Effect on organs Cardiovascular system Respiratory system Central system

17 Plays a key role in cell replication Especially relevant for the brain Neural cells multiply mainly in utero and during the first 2 years of life Fetal deficiency leads to Increased rates of spontaneous abortion Stillbirths Congenital anomalies Cretinism Psychomotor deficits Neonatal mortality

18 The spectrum of IDD The spectrum of IDD Fetus  Abortions  Stillbirths  Congenital anomalies  Increased perinatal mortality  Neurologic creatinism  Psychomotor defects Neonate  Neonatal goiter  Neonatal hypothyroidims Child & adolescent  Goitrous juvenile hypothyroidism  Impaired mental function  Retarded physical development Adult  Goiter with its complications  Hypothyroidism  Impaired mental function 18

19 IDD and selenium deficiency  Se part of peripheral type I de-Iodinase (kidney and liver)  Se deficiency: slower T4 to T3 metabolisation  Se part of Glutathion peroxidase : protector of H 2 O 2 damage Thyroid damage, disfunction of thyroid  Cerebral de-iodinase is not Se dependent  Glutathion peroxidase stimulates T4 production

20 The Recommended Dietary Allowance (RDA) Recommended Dietary Allowance (RDA) for Iodine Life Stage Life Stage Age Males (mcg/day) Males (mcg/day) Females (mcg/day) Females (mcg/day) Infants 0-6 months 110 (AI) AI 110 (AI) AI Infants 7-12 months 7-12 months 130 (AI) 130 (AI) Children 1-3 years 1-3 years 90 90 Children 4-8 years 4-8 years 90 90 Children 9-13 years 9-13 years 120 120 Adolescents 14-18 years 14-18 years 150 150 Adults 19 years and older 150 150 Pregnancy all ages all ages - 220 Breastfeeding - 290

21 Food sources FoodServing Iodine (mcg) Salt (iodized) 1 gram 77 Cod 3 ounces 99 Shrimp 35 Fish sticks 2 fish sticks 35 Tuna, canned in oil 3 ounces (1/2 can) 17 Milk (cow's) 1 cup (8 fluid ounces) 56 Egg, boiled 1 large 29 Navy beans, cooked 1/2 cup 35 Potato with peel, baked 1 medium 63 Turkey breast, baked 3 ounces 34 Seaweed 1 ounce, dried Variable; may be greater than 18,000 mcg (18 mg)

22 Goiter

23 Endemic goiter  More than 5% of the preadolescent the preadolescent (6-12 years) school (6-12 years) school age children have age children have enlarged thyroid glands. enlarged thyroid glands. 23 Simple (nontoxic goiter)

24 Endemic Cretinism (Neurologic Form)  Sever mental deficiency  Deaf mutism (Cochlear lesion)  Motor spasticity (spastic diplegia) proximal rigidity of both lower proximal rigidity of both lower and upper extremities and the trunk. and upper extremities and the trunk.  Goiter 24

25 25 Endemic Cretinism (Neurologic Form)

26 Endemic Cretinism (Myxedematous Form) 26  Less sever degree of mental retardation retardation  Sever growth retardation  Puffy features  Myxedematous and dry skin  Delayed sexual maturation  No goiter

27 27 An adult male from the Congo, with three women of the same age (17-20 years), all of whom are myxedematous cretins. Myxedematous Cretinism

28 Individuals at risk of iodine deficiency  Vegetarian and nonvegetarian diets that exclude iodized salt, fish, and seaweed have been found to contain very little iodine

29 Goitrogens  Some foods contain substances that interfere with iodine utilization or thyroid hormone production  Some species of millet and cruciferous vegetables (for example, cabbage, broccoli, cauliflower, and Brussel sprouts)  The soybean isoflavones, genistein and daidzein, have also been found to inhibit thyroid hormone synthesis  Most of these goitrogens are not of clinical importance unless they are consumed in large amounts or there is coexisting iodine deficiency  Goitrogens are inactived in heat

30 Acute toxicity&Iodine excess Tolerable Upper Intake Level (UL) for Iodine Age Group Age Group UL (mg/day) Infants 0-12 months Not possible to establish* Children 1-3 years 200 mcg/day Children 4-8 years Children 4-8 years 300 mcg/day Children 9-13 years Children 9-13 years 600 mcg/day Adolescents 14-18 years 900 mcg/day Adults 19 years and older 1,100 mcg/day (1.1 mg/day) *Source of intake should be from food and formula only.

31 Prevention

32 Prevention  Use of iodine solution(oral or injectional): -In population that incidence is >70% -If iodide salt is not available -One IM injection 0/5-1ml is sufficient for 3- 5 years -One oral dose is sufficient for 1-2 years

33 Summary of IDD Control Status in EMRO Source: Elimination of Iodine Deficiency Disorders, a manual for Health Workers: WHO, 2006

34 Recent Scenarios on IDD  There are fewer countries (47) where IDD is considered to be a public health problem in recent years.  Conversely, there is a substantial number of countries (34) where the level of Iodine intake is too high exposing susceptible groups to the risk of Iodine-induced hyper-thyroidism.

35 Urinary Iodine  Reflects directly intake  Is best to follow up programme response, goitre takes time to decrease in size  Samples needed are smaller  Technique is simple and not expensive  Samples can be taken easily, cheap, acceptable and don’t need conservation techniques

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38 جدول مقايسه اي پايش يد ادرار دانش آموزان استان يزد88-83 سالتعداد نمونه ميانگينميانهحداقلحداكثركمتر از 2 ( درصد ) 9/4 -2 ( در صد ) 9/9-5 ( درصد ) 9/19- 10( در صد ) 9/29 - 20( در صد ) بيشترا ز 30 ( درصد ) 8323957/19155/740--38/1352/74-1/12 8423598/19185/647--2/196/64-1/16 85240 15.3915.2426-2.915.850.430.80 86242 2/227/197/547--3/158/344/215/28 87240 4/165/174/334-3/3153/568/206/4 88237 6/189/211/29/41- 3/1 1 133/304/277/17

39 در كنترل اختلالات يد WHO معيارهاي در كنترل اختلالات يد WHO معيارهاي 1- مصرف نمك يددار درخانوار بيش از 90 درصد 2- يد ادرار كمتر از 10 ug/dl كمتر از 50 درصد  يد ادرار كمتر از 5 ug/dl كمتر از 20 درصد 3- اندازه تيروئيد كودكان 12-6 ساله كمتر از 5 درصد 4- TSH نوزادان بيشتر از 5 ميلي واحد/L كمتر از 3 درصد

40  كميته كشوري پيشگيري از اختلالات ناشي از كمبود يد در سال 1367 شكل گرفت.  اعضاي كميته كشوري در سال 1368 اولين برنامه 5 ساله پيشگيري از اختلالات ناشي از كمبود يد را تدوين كرد.  همزمان با تشكيل كميته كشوري، اولين بررسي كشوري براي تعيين شيوع گواتر در استانهاي كشور انجام شد.  برنامه 5 ساله سوم (1382-1378) در تيرماه 1378 بر اساس وضعيت موجود برنامه تجديدنظر شد.

41  هدف کلي استمرار پيشگيري وکنترل اختلالات ناشي ازکمبود يد  اهداف اختصاصي حفظ وارتقا ميزان دسترسي ومصرف نمک يدداردربيش از 90% خانوارها حفظ ميزان يدادراردرطيف 30-10ميکروگرم دردسي ليتر حفظ وارتقاتوليد وتوزيع نمک يدداربا کيفيت مطلوب

42 راهکارها راهکارها  کنترل کيفيت توليدوتوزيع نمک يددار  آموزش هاي همگاني وبازآموزي  اندازه گيري ميزان يدادرارکودکان10-8ساله براي اطمينان ازدريافت يدکافي درمقاطع يک ساله  پايش روندکيفي وکمي برنامه  ارزشيابي برنامه

43 اعضاي كميته استاني IDD  معاونت بهداشتي دانشگاه مربوطه (مسئول و رئيس كميته استاني IDD)  كارشناس مسئول بهداشت خانواده  كارشناس مسئول تغذيه معاونت بهداشتي دانشگاه (دبير كميته IDD)  كارشناس مسئول آموزش بهداشت  رئيس اداره نظارت بر مواد غذايي دانشگاه

44 اعضاي كميته استاني IDD  كارشناس مسئول آزمايشگاه مواد غذايي دانشگاه  كارشناس مسئول گسترش شبكه هاي بهداشتي درماني  كارشناس مسئول بهداشت محيط با مدير گروه بهداشت محيط و حرفه اي استان  نمايندگان ديگر كه بر اساس شرايط خاص حضور آنها ضروري بنظر رسد.

45 6/4/201645


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