1. Iodine deficiency disorders zIodine is an essential component in thyroid hormone production zThyroid hormone regulates basic metabolism :energy consumption, cellular activity, growth and in particular brain development. zHypothyroidism: slow, cold, sluggish brain function, short stature, mental and motor development delayed or slowed. In extremes general neurological development delayed.

4. Hormone regulation

5. Hormones and iodine deficiency

6. Spectrum of disease

7. Importance of the problem

8. Prevalence z1 billion persons exposed z200 million persons affected (goitres) z26 million cases of mental problems z6 million cases of cretinism

9. Goitre  Increase in size four to five times distal phalanx of the thumb  Aesthetic  Compression  Related hypothyroidism: is not a compensation  cancer zIod Basedow (hyperthyroidism) due to hyperstimulation, mutation autonomous nodules

20. Iodine deficiency and the foetus zBrain development fast between 3-5 months pregnancy and from third trimester till end of second year zMaternal T4 essential for first 24 weeks zFoetal T4 starts at 24 weeks z30% cord blood is of maternal origin

22. Iodine and the neonate zPerinatal mortality zInfant mortality zLow birth weight zBrain development needs T4 zIodine deficiency mental retardation, retarded motor development. zGeneral IQ decrease of 15 Points

23. Iodine deficiency and adults zLack of energy zapathy, slow brains zgoitre and mechanical complications zNodular thyroid zhyperthyroidism zPregnancy and cretinism

24. Aethiology zLow iodine uptake. Soil dependent yerosion, wash away: deltas zGoitrogens yManioc: linnamarin thiocyanate xBlocs uptake of Iodine at the thyroid, competitive inhibition xTraditional preparations xKonzo yBrassica family ypolutants

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

29. Iodine needs

30. Diagnosis of endemicity zPrevalence of goitre zDosage of urinary iodine zTSH dosage zPrevalence of cretinism

31. Prevalence of goitre

33. Urinary Iodine zReflects directly intake zIs best to follow up programme response, goitre takes time to decrease in size zSamples needed are smaller zTechnique is simple and not expensive zSamples can be taken easily, cheap, acceptable and don’t need conservation techniques

35. Endemic cretinism zNeurological ySevere motor and mental deficit ycerebral palsy ydeafness, mutism yeuthyroid zMyoedematous ySevere mental deficit yHypothyroid, destruction of the thyroid yIodine deficiency combined with goitrogens and Se deficiency

49. Control strategies zSupplementation: injections, oral zFortification zchanging food habits

50. Supplementation zNeed to start early in pregnancy zsupplement women of child bearing age zOperational difficulties zInjections and hepatitis and HIV zCovers need for about 4 years injections zOral covers needs for one year

51. Fortification zAdd iodine to a vehicle: salt or water zAdditive must be stable, not change the carrier zNo by-pass, centralised production zNeed for a comprehensive approach zPackaging, evaporation zAccess of all the population to the fortified food zPolicy and protection of the market zWho pays? zSuccess story of Iran

53. Food habits zVery limited approach, food reflects iodine soil content

54. Control complications zNeed for intensive follow up zChanging consumption patterns in salt zVariations in salt consumption zTransient hyperthyroidism