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Iodine Deficiency Disorders  : Past , Present and Future

 

 

 

 

 
 
 

 

 


Dr. Umesh Kapil, Additional Professor

Dept. of Human Nutrition,

AIIMS New Delhi.

e mail  :  kapilumesh@hotmail.com

 

 

 

History  of  IDD

Endemic goiter in India is an age-old problem. There are references to it in ancient Hindu scriptures dating back to 2000 B.C . “Tumors” of the neck, generally regarded as thyroid swellings, have been described by the Hindu physician Charaka and the surgeon Sushrutha in their treatises from about 600 B.C. The inhabited valleys of the Himalayas  has  long been regarded as one of the world’s classic and most intense areas of endemic goiter. Sir Robert McCarrison labored for nearly 30 years in the early part of  twentieth  century in search of the causative factors  of this  endemic. Subsequently  he  propounded the theory that this endemic was of complex derivation, being related to “Goiter Noxa” and faulty and deficient diets . The recent studies  of  thyroid physiology  utilizing the  help of   radioactive iodine has finally   confirmed  that  the iodine deficiency is the primary cause of IDD in India.

 

 

Magnitude of  IDD

Iodine Deficiency Disorders is known to be a significant public health problem in 118 countries. At least 1572 million people worldwide are estimated to be at risk of IDD i.e. who live in areas where iodine deficiency is prevalent (total Goiter rates above 5%), and at least 655 million of these are considered to be affected by Goiter. A recent WHO/ UNICEF/ICCIDD report estimates that currently  about  29% of the world's population live in areas of iodine deficiency and need some form of iodine supplementation.  Most of these are in developing countries in Africa, Asia, and Latin America, but large parts of  Europe  are also vulnerable.

 

About 200 million people are  at  the risk of IDD in India. The survey conducted by the Central and State  Health  Directorates,  ICMR , other   Medical  Institutes  have clearly demonstrated that not even a single State/UT is free from the problem of IDD. Sample surveys  conducted in 25 States and 4 UTs of  the country have   revealed that out of 282 districts surveyed so far, IDD  is a  public health problem in 241 districts ,with  the prevalence  of  more than 10 per cent. ( Table I). It is estimated  that 71 million population are  suffering from goiter and other  IDD. 

 

 

Etiology

Iodine is one of the essential elements required for  normal human growth and development.   Its daily per capita  requirement is 150 micrograms. Soils from mountain ranges, such as the Himalayas, Alps, and Andes,  and from areas with frequent flooding,  are  particularly likely  to  be  iodine deficient. The problem  is  aggravated  by accelerated  deforestation and soil erosion.  The food grown in iodine  deficient regions  can  never provide enough iodine to the  population  and live-stock living there. Unlike  nutrients  such as iron, calcium  or  the  vitamins, iodine does not occur naturally in specific foods; rather, it  is present  in the soil and is ingested through foods grown on  that soil.  Iodine  deficiency  results  when there is lack  of  iodine  on  the earth's  crust .  Living on the sea coast does not guarantee iodine sufficiency  and  significant pockets of iodine  deficiency  have been  reported  from  the Goa, Bombay, Kerala,  and  Andaman  and Nicobar Islands. Even those areas which are presently relatively free of this problem can become endemic because of intensive agricultural technologies and subsequent depletion of soil with iodine and soil depletion. India  do not   have a alternative but  to intensify agricultural operations in order to increase the yield of food per unit of land to meet the growing needs of population.

 

The  contribution  of  different food groups  to  the  daily intake  of iodine are cereals 40 percent, milk and milk  products 37  percent,  flesh  foods  11 percent,  pulses  10  percent  and Vegetables  2  percent. Cereals and  pulses  together  contribute significantly to the daily intake of iodine .

 

Iodine deficiency thus results mainly from geological rather than  social and economic conditions. It cannot be eliminated  by changing  dietary  habits or by eating specific  kinds  of  foods grown in the same area . Besides nutritional iodine deficiency,  a variety  of  other  environmental,  socio-cultural  and  economic factors  operate  to  aggravate  iodine  deficiency  and  related thyroid  dysfuncitons.   These include poverty  related  protein-energy  malnutrition,  ingestion of  goitrogens  through  unusual diets (particularly by the poor), bacteriologically  contaminated drinking  water,  as  well  as bulky  high  residue  diets  which interfere  with  intestinal absorption of iodine.

 

There  is  also evidence  to believe that intensive cropping, resulting in  large scale removal of biomass from the soil, as well as widespread use of  alkaline fertilizers, rapidly deplete the soil of its  iodine content.   Since  both  intensive cropping and  use  of  alkaline fertilizers  are  widely practiced in almost all  states  of  the country, it is not surprising that nutritional iodine  deficiency and endemic goiter are seen wherever they are looked for in India 

 

Several environmental and genetic factors interfere with the above   processes  of  thyroxin  synthesis  leading   to   goiter formation.   The genetic factors, which are rare,  mainly  affect the  enzymes  involved  in  thyroxin  synthesis.    Environmental factors  are  amongst the most common factors that  interfere  in thyroxin  synthesis  and  lead to  goiter  formation.   The  most important  environmental  factors are  (i)  environmental  iodine deficiency (ii) goitrogens.  However, the most frequent cause of  goiter  in  India  and  other countries is  environmental   iodine deficiency.   However, there is emerging evidence in India that  goitrogens  may  be playing a  secondary  role  in  several endemic  foci.   Goitrogens are chemical substances,  that  occur primarily  in  plant food.  They can occasionally be  present  in contaminated  drinking water.  Goitrogens interfere  in  thyroxin synthesis by inhibiting the enzymes involved in the synthesis  of thyroxin.

 

Besides iodine deficiency and goitrogens, a variety of other factors  can  adversely affect efficient thyroxin  synthesis  and iodine  utilisation  in  the body, resulting  in  aggravation  of goiter.    These  include, protein energy  malnutrition,  dietary factors  that  interfere with iodine absorption etc. Environmental iodine deficiency coupled with a variety of ancillary factors compromises thyroxin biosynthesis which results in prevalence of endemic goiter .

 

Iodine  deficiency  in  food and water leads to  less  iodine  to thyroid  gland which is the exclusive organ for synthesis of  two very important iodine containing hormones T3 (Tri iodo thyronine) and T4 (Thyroxin).  As a result, the thyroid gland becomes  hyper active  to  produce the requisite amounts of T3  and  T4  thereby enlarging  itself by hyperplasia phenomenon under compulsion  and this enlargement of the thyroid gland is known as goiter.  In the past,  goiter  was said to be a cosmetic problem however the   recent research studies   have shown that goiter is one of the several  disorders that the body is subjected to suffer due to iodine deficiency.  All the disorders are currently being categorised under a term Iodine deficiency  disorders (IDD). The  relationship between dietary  iodine intake and  severity of IDD is shown  in Table-II.  

    

The major factors responsible for iodine deficiencies are :

 

  • Recurrent flooding in the areas.
  • Heavy rainfall /snowfall
  • Removal  of great amount of biomass  due  to  multiple crops.
  • Goitrogens in food, monotonously consumed by the poor.
  • Bacterial load of water, poor sanitation,
  • PEM and recurrent infection due to poverty.

 

 

Health Consequences of  Iodine Deficiency   

Iodine deficiency has been called the world's major cause of preventable mental retardation. Its severity can vary from mild intellectual blunting to frank cretinism, a  condition  that includes  gross mental retardation, deaf mutism,  short  stature, and various other defects. In areas of severe iodine deficiency, the majority of individuals risk some  degree  of  mental impairment.  The damage to the developing brain results in individuals  poorly  equipped  to  fight  disease,  learn,   work effectively, or reproduce satisfactorily.The  spectrum  of  disorders  caused  due  to  iodine deficiency  affects all the stages of life- from fetus  to  adult (Table III).If  a  pregnant woman diet do not   contain  adequate iodine, the fetus cannot produce enough thyroxin and fetal growth is  retarded.  Hypothyroid fetuses often perish in the  womb  and many infants die within a week of birth. The current data on the embryology of the brain suggest that the  critical  time for the effect of iodine  deficiency  is  the mid second trimester i.e. 14-18 weeks of pregnancy. At this time  neurons of  the cerebral cortex and basal ganglia are formed. It is  also the  time of formation of `Cochlea' (10-18 weeks) which  is  also severely  effected in endemic cretinism. A deficit in  iodine  or thyroid  hormones  occuring during this critical period  of  life results  in the slowing down of the metabolic activities  of  all the  cells  of the  fetus and irreversible alterations  in  the development  of  brain.  The growth and  differentiation  of  the central  nervous  system are closely related to the  presence  of iodine and thyroid hormones. Hypothyroidism may lead to  cellular hypoplasia  and  reduced  dendritic  ramification  gemmules   and interneuronal  connections. Hypothyroid   children   are intellectually subnormal and may also suffer physical impairment. They  lack the aptitudes of normal children of similar  age,  and are often incapable of completing school. Studies have documented that  in areas with an incidence of mild to moderate IDD, IQs  of school  children  are,  on  average, 10 –12  points  below  those  of children living in areas where there is no iodine deficiency. Foetal thyroid start secreting thyroxin early in  the 2nd  trimester in intra-uterine life.  From then on till the  end of  the  first  year of post-natal life, thyroxin  plays  a  very important  role  in the growth and functional maturation  of  the fetal brain.   Thyroxin  deficiency  during this  critical  period  can result  in impaired brain development which cannot  be  corrected later by giving iodine or thyroxin.

 

The  thyroid  gland  in its present form  evolved  over  the course of millions of years of biological evolution. The molecule of  thyroxin has four atoms of iodine.  Therefore, iodine  is  an essential  element required for the synthesis of  thyroxin.   The thyroid gland has very efficient mechanisms for extracting iodine from  the  circulation,  where  it may be present  in  as  low  a concentration  as  0.01  micrograms per 100 ml  of  plasma.   The minimum  daily requirement of iodine by thyroid gland in  man  is estimated to be 100 micrograms.  To extract this amount of iodine from  the circulation, the thyroid daily clears several  hundreds of  liters  of  plasma of its iodine.   This  work  can  increase further   by   several  times  in   severely   iodine   deficient environments  because  of the very low concentrations  of  iodine present  in the circulation in such conditions.  To cope up  with this increased work load, the thyroid enlarges in size, under the influence of thyroid stimulating hormone (TSH), secreted from the pituitary gland.  The efficient compensatory mechanism  triggered by  low  thyroxin feedback at the hypothalamic  centers  lead  to increased  TSH secretion from the pituitary and cause  remarkable enlargement of the thyroid gland resulting in goiter . Iodine as iodide (I-the ionic form) is transported into  the cells  by  the iodide pump.  This process is  called  `trapping'.  The trapped `iodine' is enzymatically oxidised to free iodine and chemically  linked  to  a  protein in  the  thyroid  cell  called thyroglobulin.   In fact the iodine is attached to the  tyrosines (an amino acid) of the thyroglobulin molecule.  The thyroglobulin so iodinated is secreted into the thyroid follicles.  Thyroxin is formed,  iodinated  and stored in  the  thyroglobulin  molecules.  Under the influence of TSH, the thyroxin stored as  thyroglobulin in the thyroid acini is released, in accordance with the needs of the  body. Synthesis  of thyroxin in the thyroid cells involve  availability of  enough iodine to the thyroid,  as well as action of a  variety of  enzymes  in the thyroid.   If  any  of  these process  is affected thyroxin  synthesis is impaired  and  goiter formation results.

 

i. Endemic cretinism

Endemic  cretinism is the extreme clinical manifestation  of severe  hypothyroidism  during  fetal,  neonatal  and  childhood stages  of  development.   It  is  characterised  by  severe  and irreversible  mental  retardation,  short  stature,  deaf-mutism, spastic  dysplegia  and squint.  In early eighties in many  seriously endemic  Tarai districts of north India,  average prevalence of 1-2% of  cretinism was seen. The  situation  has improved significantly  with  supply  of iodised salt and the cretins are no more born.

    

Cretinism  seen  in endemic areas is  predominantly  of  two types  (a)  Neurological cretinism, where only  the  neurological manifestations  of thyroxin deficiency early in life  (in  utero) and  dysplegia  and squint. This  is  presumably  because,  in  such  individuals hypothyroidism was confined to the in-utero or neonatal stages of life.   (b)  Myxedematous cretinism where besides  having  mental retardation,  have  myxoedema  and dwarfism.  This variant of  cretinism is  presumably because of continuing hypothyroidism  through all phases of life.

 

ii)  Cretinoids

Besides  the  few  who manifest as cretins,  in  an  endemic goiter area, a large number of individuals with lesser degrees of mental  retardation,  speech  and  hearing  defects,  psychomotor retardation,  as  well  as  gait  defects  may  be  seen.    Such individuals   are  known  as  cretinoids.   The   prevalence   of cretinoids may be tenfold or more, than fully manifested  cretins in severely endemic regions.

 

iii) Other syndromes due to foetal iodine deficiency

There is   preliminary scientific evidence suggesting that severe  iodine deficiency  can lead to  fetal wastage  such  as abortion,  still births, and congenital abnormalities.   However, hard evidence available in this regard is limited.

 

 iv)  Neonatal and childhood hypothyroidism

When  the  cause  of endemic goiter  in  the  Himalayas  was investigated  in the late fifties, modern techniques for  precise measurement  of  thyroid  hormones were not  available.   In  the sixties, and seventies, when radio-immunoassay techniques  became available   for  sensitive  and  precise  measurement  of   these hormones,  it  was  discovered that more than  30%  the  goitrous subjects  in  endemic areas were functionally  decompensated  and hypothyroid  despite  the `adaptive' enlargement of  the  thyroid. Subsequently, in early eighties by screening the  cord blood of over 20,000 newborns, it was discovered that one out  of every 10 new borns from the Tarai regions of UP were  hypothyroid at birth.  

 

iv)   Adult Hypothyroidism

A large number of goitrous adults in  an endemic region can have varying degrees of hypothyroidism leading to a variety of clinical symptomatology and complications related to  hypometabolic  states.  These  symptomatology  can  seriously hamper  human energy and work capacity with resultant erosion  of economic  productivity of endemic regions.  Indeed  such  factors may   possibly  be  contributing  to  the  known   socio-economic backwardness  of  endemic regions.

 

v)  Goiter and its complications

These are well known medical and surgical problems which are also included in the syndrome of IDD.  Besides, there is emerging epidemiological  evidence  linking  endemic  goiter  with  incidence thyroid cancer.

 

 

National Iodine Deficiency Control Program

Following the successful trial of iodized salt in the Kangra valley, Himachal Pradesh, a National Goiter Control Program was launched  by the Government of India in 1962. 

 

Objectives : National IDD Control Program has the following objectives:

  • Initial  surveys  to assess the  magnitude  of  the  iodine deficiency  disorders.
  • Supply of iodised salt in  place  of common salt.
  • Resurveys to assess the impact of iodised salt after  every 5 years.

 

 

Beneficiaries

All  people  residing in endemic and non-endemic  areas  for IDD.  The  population  in  known endemic  area   are  given priority.

 

Activities  and Services provided under  the  NIDDCP:

 

The following activities are  conducted under the NIDDCP:

 

i.  Production and Distribution of Iodised Salt

On the recommendations of Central Council of Health in 1984, the  Government took policy decision to iodise the entire  edible salt   in  the  country.   This  policy  decision   was implemented w.e.f.  April, 1986 in phased manner. Subsequently the e iodised salt production  was liberalized to private sector. Six  hundred fourth  one  private  manufactures have  been  licensed  by  Salt Commissioner  . These have annual production  capacity  of iodised  salt of more than 60 lakh tons  (which is  adequate  for the  entire country). The annual production of iodised  salt  has increased  from 5 lakh metric tons in 1985-86 to 45  lakh  metric tons  in  1998-99.  This is expected to further rise furthur  to  52  lakh metric tones in near future which is the  projected national requirments .

 

Budget  is  provided  to  Salt  Deaprtment   for monitoring the  quality  control of iodised  salt  produced  at production level.  The Salt Commissioner in consultation with the Ministry  of  the  Railways arranges for  the  transportation  of iodised salt from the production centres to the consuming  States under  priority  category  `B', a priority  second  to  that  for defence  .The   Salt  Deaprtment has   been initiating action to improve packaging of iodised salt to  prevent iodine loss during transit. The State Government have been advised to include iodised salt under Public Distribution System (PDS).

 

ii.  Notification for banning use of non-iodised salt

To  ensure use of only iodised salt the sale of  non-iodised salt  has  been  completely  banned  under  Prevention  of   food Adulteration  Act,  1954, in all states and   union  territories. However there  is  no ban notification in state of  Kerala.  Realizing  the  importance of iodine deficiency  in  relation  to human resource development, NIDDCP has been included in 20  point Program of  the Prime Minister for monitoring the progress.

 

iii.   Establishment of Goiter Cell :

For effective monitoring and proper implementation of  NIDDCP, all the States and UTs have been advised to establish IDD control Cell  in  the  State  Health  Directorate.  Government  of  India provides budget for this purpose.  Presently ,26 States and  Union Territories  have established NIDDCP Cells

 

iv.   Information education and communication activities

Central  Government provides cash grants to the  states  and UTs   for production of health education  material  and  carrying out    health  education  activities  on  IDD  as  well  as   for undertaking  IDD  surveys.  To intensify  the  IEC  activities  a communication package by way of video films, posters/danglers and radio/TV  spots  has  been produced. TV  video  Spots  are  being regularly telecasted through the National Network of  Doordarshan about the consequences of Iodine Deficiency  and the benefits  of consuming iodised salt.  

    

The  standards  for iodised salt have been laid  down  under PFA,  1954.   These stipulate the iodine content of salt  at  the production  and consumption level to be at least 30 and  15  ppm, respectively.  Under a GOI-UNICEF project  intensive monitoring  and  IEC  activities  have  been  undertaken  in  selected  districts of  India.

 

v.   Intersectoral Co-ordination :

It   has  been  realised  that  NIDDCP  activities   require integrated efforts of multiple agencies like Industry,  Railways, Health,  Education,  Food  and Civil  Supplies,  Information  and Broadcasting   etc.  The focus of NIDDCP activities has now  been shifted    from   only    health   department   to   multi    and interdisciplinary participation.

 

vi.  Laboratory Support:

A  National Reference Laboratory for monitoring of  IDD  has been  set up at the Bio-chemistry division of National  Institute of   Communicable  Diseases,  Delhi  for  training  medical   and paramedical  personnel and monitoring the iodine content of  salt and urine.

District  level IDD monitoring laboratories are being  setup in   all   the   States  for estimation of iodine content of salt  and urinary  iodine excretion. These two laboratory investigations  are the most effective tools  for proper monitoring the  implementation  of  IDD  Control  Program. For  ensuring  the  quality  control  of  iodised  salt  at consumption  level,  testing kits for "on the  spot"  qualitative testing   have   been   distributed  to   all   District   Health Functionaries for creating awareness about consumption and use of iodised salt.

    

vii.  Training  under NIDDCP Programs :

Every year, training Programs are conducted  in management and  monitoring of National Iodine Deficiency Disorders Control Program  for the Regional  Directors of Health and Family Welfare and   the State  level technical officers  by the Directorate General of Health Services. Training  Programs  for laboratory technicians  from  the state  level IDD monitoring laboratories are also   organised  by the Directorate General of Health Services every year.

 

viii   Evaluation:

The  status of salt iodisation in different states has  been extensively  assessed  by different research  studies  and by national level surveys in  recent years . The NFHS‑2  was one of the klargest suvey which covered all the states in the country with a representative sample of households . Thee degree of  iodization of salt used in households was assessed. It was found that more than 70% population was consuming iodised salt. ( Table IV).The  research studies  conducted has identified following areas  which  require strengthening :-

 

  • Irregular distribution of iodised salt for varying  periods

 

  • Lack of monitoring of quality of iodised salt distributed.

 

  • Failure  of lifting of allotted quotas of iodised  salt  by wholesale agents for further
  • distribution to  retailers.

 

  • Inadequate  coordination  between  salt  dealers  and   food inspectors  ( the implementors
  • of PFA  Act)causing  disruption  in the sale of  iodised salt.

 

  • Poor coordination between  various departments like Food  and Civil Supply, Health,
  • Industry, Railways.

 

  • Non - issue complete ban notification by all  the States for  the sale of non-iodised salt.

 

  • Non-establishment  of  IDD  Control  Cell  in all the  States/UTs.

 

  • IDD Monitoring Laboratories is yet to be  set up  by  all the States.

 

  • Inadequate   enforcement  of  PFA  act  by  the   State/UT Governments  to ensure the
  • quality of   iodised salt is  available to the consumer

 

Regular  IDD  surveys  are not  conducted  by  the  State/UT Governments  to  monitor  the progress/identify  new  areas   of endemicity.

 

 

Safety of Iodised Salt

Iodine  requirements  have  been  calculated  based  on  (i) average daily physiological loss of iodine in the urine which  is 100-200 mcg/ day and (ii) balance studies to get  equilibrium or  positive  balance which is 44-162 mcg/ day. These studies have estimated  a safe daily intake of iodine  between  a minimum of 50 mcg and a maximum of at least  1000  mcg. The  generally accepted desirable adult intake  is  100-300 mcg/day. In India  the  current recommended dietary  iodine intake for adult  is 150 mcg/ day.

 

The  average salt intake among adults is about 10g/day,  and at  the  current level of fortification of salt with 15  ppm   of iodine at the consumer level , the iodised salt  provides an  additional  amount  of  about  73.5  mcg  only   (considering the losses   during  cooking  and  biologically  available).   The remaining requirement of iodine is met from the dietary  sources. Thus, the total intake of iodine is much below the safe limit and therefore  the  iodised  salt is unlikely to  cause  any  harmful effects even in populations who are not iodine deficient. Also It has been documented that at all intake levels, a proportionate amount of  iodine is  excreted  in the urine.

 

The  recent research studies conducted by Human Nutrition Unit ,AIIMS New  Delhi amongst  the children  have clearly documented that the UIE levels  are within the Physiological limits i.e. 100 mcg to 200 mcg per liter. Also, an analysis of more than  10,000  salt samples  collected from different parts of country revealed  that only 2.5% of salt samples had iodine content of more than 60  ppm and  82%  had less than 45 ppm . These findings indicated  that currently   fortification  of salt  with  iodine  is  done as  per  the  recommended  norms  of Government of India. In view of all scientific evidence the iodised salt is safe.

 

 

Assessment of  IDD 

 

i. Sampling Procedures

Probability  Proportionate to Size(PPS) cluster sampling  methodology is recommended. The thirty clusters is should be  covered and should be selected as follows. Firstly  all   population  units/villages in the area to surveyed is  listed  along  with  the population. Secondly ,the  cumulative frequency table is prepared and  the  total population in the survey area is calculated. Then by dividing total population with 30, the sampling  interval  is calculated.  Subsequently the  first  cluster  is  selected  at  random   and subsequent clusters are calculated by adding sampling  interval.  The  number of  subjects  to be surveyed within  each  cluster depends on the following :i. estimated prevalence of IDD, ii. level of precision desired, iii. variability of prevalence between clusters

 

ii. Selection of Target Groups for IDD  Survey 

The survey should be conducted  in  a  sample of  population which should be  representative of the population. The school age children reflect the IDD status of   the community, are vulnerable to deficiency and respond to the iodine supplementation intervention and hence have been recommended  for the survey

 

iii. Indicators for Assessing IDD:

 

The  common indicators for assessment of IDD are i. Clinical indicators  and Biochemical indicators. It is recommended that the assessment of iodine content of salt consumed by the subjects should also be included in the survey as  data on this aspect provides the guideline for developing the intervention for prevention of IDD simultaneously.

 

 

iv. Clinical  Indicators

 

Thyroid size

The size of the thyroid gland changes inversely in  response  to  alterations  in iodine intake, with a lag of 6-12  months  in children and young adults (i.e <30 years of age). The traditional  method for determining thyroid size is inspection and  palpation. Palpation of the thyroid is important in  assessing  Goiter prevalence. Costs is minimal. It is   relatively  easy to conduct. The training of personnel can be done. Children 6-12 years of age should be studied. Very young children have  smaller  thyroid and it is  more difficult it is to  perform  palpation.  It is recommended that if the proportion of children attending school is less than 50%,spot surveys should be done  on two  groups  of children of the same age, i.e  those  who  attend  school  and  those  who  do not, to ascertain  if  there  is  any significant difference between the two. If so, both groups should  be  studied  separately,  in  all  clusters,  or  an  appropriate  adjustment  should  be  made  in  the  rate  found  among  school  children. 

 

A modification of the previous Goiter classification system,  which  defined five grades, is recommended. The  previously  used  grades  1A and 1B are thus combined into one, and grades 2 and  3  are   combined  into  another  (Table  V).  Table  VI  gives   the epidemiological  criteria  for establishing IDD severity  based  on Goiter prevalence in school age children. It  is  recommended that a total  Goiter  rate  (TGR, Goiter  grades  1 and 2 ) of 5% or  more in primary school  children  (age  range approximately 6 to 12 years) be used to signal the presence of  a public health problem. This recommendation is based on  the observation  that  in  a normal, iodine  replete  population  the prevalence  of  Goiter  should be quite low. The cut  off  of  5% allows  some  margin of inaccuracy of Goiter assessment  and  for Goiter that may occur in iodine replete population due to  other causes  such as goitrogens and autoimmune thyroid  diseases.  The previously  recommended  10%  cut  off  level  has  been  revised downwards  since it has been shown that Goiter  prevalence  rates between   5%  and  10%  may  be  associated  with  a   range   of  abnormalities,  including  inadequate  urinary  iodine  excretion and/or  sub  normal  levels of TSH  among  adults,  children  and  neonates.  The  specificity and sensitivity of palpation  are  low  in  grades  0  and  1  due to a high  inter  observer  variation.  As demonstrated by studies of  experienced examiners,  misclassification can be as high as 40%. Measurement of  urinary  iodine levels (in an adequate sample) essential to  decide  whether  an  iodine  deficiency  problem  is  of  public   health  importance.

 

v. Biochemical Indicators

 

Urinary  Iodine

Since most iodine that is absorbed is excreted, therefore the urinary iodine level is a good marker of a previous day's dietary iodine intake. However, since an individual's level of urinary iodine varies daily and even during a given day, data can be used only for making a population based estimate. Experience has shown that the iodine concentration in early morning urine specimens (child  or  adult)  provides  an  adequate  assessment   of   a population's iodine status; 24-hour samples are not necessary. Acceptability is very high and spot urine specimens are easy to obtain.  Urinary iodine assay methods are not difficult to learn or use, but meticulous attention is required to  avoid contamination with iodine at all stages. Special rooms, glassware and reagents should be set aside solely for this purpose.

 

Small amount (0.5-1.0ml) of urine is required. Specimens are collected in tubes, which are tightly sealed with screw tops they do not  require  refrigeration  or  the  addition  of   a preservative. Iodine content remains stable throughout transport to the laboratory. The  tightly sealed  specimens  can  be refrigerated  in the laboratory for several months before  actual determinations   are  made.  Should evaporation occur, iodine concentration will increase.

Since casual specimens are used, it is desirable to measure about 300 from a given population group to allow for varying degrees of subject hydration and other biological  variations  between  individuals,  as well as to obtain  a  reasonably  small  confidence  interval.  Smaller sample sizes are adequate to establish at the outset that iodine deficiency is the cause of the endemic Goiter. The  cut  off points proposed for classifying  iodine  deficiency into different degrees of public health significance are shown in Table  VII.  Frequency distribution curves are necessary  for  full interpretation, since urinary iodine values from populations  are usually  not normally distributed and therefore the median  value should  be  used rather than the mean. The  indicator  of  iodine deficiency   "elimination"   is  a  median   value   for   iodine concentration of 100 ug/l, i.e 50% of the samples should be above 100  ug/l, and not more than 20% of samples should be  below  50 ug/l.  As  an IDD prevention Program  progresses,  Goiter  rates become  progressively  less  useful, and  urinary  iodine  levels progressively more useful, as elimination criteria.

 

 

New  frontiers in  the field of  IDD

A disturbing finding in recent years is the emergence of new goiter-endemic areas in the irrigated plains of  country. The precise factors underlying this have not been identified; but  it is  being  suspected  that  the  modern  practice  of   intensive agricultural  technology  could have resulted in  the  diminished bioavailability  of  soil iodine and  the  consequent  diminished content of iodine in food and water.      The  possible  role  of an  excessive  use  of  fertilisers, pesticides and food additives has also been suspected. The  possibility  that  goitrogens  may   be involved  in  the  emergence  of  new  goiter-endemic  areas   is suggested  by the finding of high levels of urinary excretion  of thiocyanate  in  a significant proportion of  subjects  in  these areas.   Peroxidase  inhibiting  goitrogens have been  suspected  to interfere with the effective utilisation of iodine by the thyroid gland.   Such goitrogens could be either present in foods  or  as food contaminants. The possible role of selenium deficiency in aggravating  the goiter problem also requires investigations. It  is  becoming  clear that problems of  iodine  deficiency  are acquiring new dimensions in the context of intensive agricultural technology and ecological and environmental factors incidental to 'development'  In combating these new dimensions we may  have  to look  for  strategies  other  than (and  over  and  above  )  the conventional  approach of the fortification of common  salt  with  iodine.

 

 


Table I

 

Prevalence  of  Iodine Deficiency  Disorders  in  Different
     States/UTs of India

 

State

Total No.

of     Districts

No. of District Surveyed

No. of  District Endemic

Andhra Pradesh

23

7

6

Arunachal Pradesh

10

10

10

Assam

18

18

18

Bihar

38

22

21

Goa

2

2

2

Gujarat

19

16

8

Haryana

16

8

8

Himachal Pradesh

12

10

10

Jammu & Kashmir

15

14

11

Karnataka

20

17

6

Kerala

14

14

11

Madhya Pradesh

45

16

16

Maharashtra

31

29

21

Mizoram

4

4

4

Manipur

8

8

8

Meghalaya

5

2

2

Nagaland

7

7

7

Orissa

30

2

2

Punjab

12

3

3

Rajasthan

27

3

3

Sikkim

4

4

4

Tamilnadu

21

12

12

Tirpura

3

3

3

Uttar Pradesh

67

34

29

West Bengal

18

5

5

Andman & Nicobar Islands

2

Survey not done

Survey not done

Chandigarh

1

1

1

Dadar & Nagar Haveli

1

1

1

Delhi

1

1

1

Daman & Diu

1

1

1

Lakshwadeep

1

Survey not done

Survey not done

Pondicherry

4

Survey  not done

Survey not done

Total No.  of District

480

282

241

 


     

Table II

 

RELATIONSHIP BETWEEN IODINE INTAKE AND IDD    

--------------------------------------------------  -------------------  

Nutritional Status           

Daily                                             iodine intake                                      

(micrograms)    

-------------------------------------------------------------  ---------

     Associated with cretinism       20 or less

     Associated with goiter              20 - 50

     Marginal                                     50 - 100

     Normal                                      100 - 300

     More than normal                   300 and above

     ---------------------------------------------------------------------


 

Table  III

 

The Spectrum of Iodine Deficiency Disorders

 

________________________________________________________________

 

Stage in Life                                                                Health Effects

________________________________________________________________

 

Foetus                                                                                     Abortions

                                                                                    Stillbirths

                                                                                    Congenital Anomalies

                                                                                    Increased Perinatal Mortality

                                                                                    Increased Infant Mortality

                                                                                    Neurological Cretinism :

 

mental deficiency

-          deaf-mutism

-          spastic diplegia

-          squint

 

    Myxedematous Cretinism :

 

-          mental deficiency

-          dwarfism

 

                                                                                    Psychomotor Defects

 

Neonate                                  Neonatal goiter

                                                                                    Neonatal hypothyroidism

 

Child and Adolescent             Goiter

                                                                                    Juvenile hypothyroidism

                                                                                    Impaired mental function

                                                                                    Retarded physical development

 

Adult                                                                           Goiter with complications

                                                                                    Hypothyroidism

                                                                                    Impaired mental function

____________________________________________________________________                   


 

Table IV.

                         STATUS OF SALT IODISATION IN INDIA  

                   

                             1998-99 NFHS   SURVEY - 2

 

Percent distribution of households by degree of iodization of salt, according to state, India, 1998–99

State

Not iodized

7 ppm

15 ppm

30 ppm

Missing

Total percent

 

India

 

North

  Delhi

  Haryana

  Himachal Pradesh

  Jammu & Kashmir

  Punjab

  Rajasthan

 

Central

  Madhya Pradesh

  Uttar Pradesh

 

East

  Bihar

  Orissa

  West Bengal

 

Northeast

  Arunachal Pradesh

  Assam

  Manipur

  Meghalaya

  Mizoram

  Nagaland

  Sikkim

 

West

  Goa

  Gujarat

  Maharashtra

 

SOUTH

  Andhra Pradesh

  Karnataka

  Kerala

  Tamil Nadu

 

  28.4          21.6        16.8        32.6         0.7        100.0

 

                                                                                      

    6.1            4.5        13.5        75.7         0.1        100.0

  19.5            9.2        13.9        57.1         0.2        100.0

    3.2            6.2        14.9        75.6         0.1        100.0

  24.8          22.3        27.5        25.4         0.0        100.0

  16.7            7.8        13.7        61.6         0.3        100.0

  37.1          15.3        21.9        24.4         1.3        100.0

 

 

  25.0          16.3        14.4        42.3         2.1        100.0

  22.7          26.9        19.6        29.2         1.6        100.0

 

 

  22.9          30.1        26.6        20.4         0.0        100.0

  29.6          35.1        18.2        16.8         0.4        100.0

  11.3          26.5        25.8        36.0         0.5        100.0

 

 

    0.8          15.0        46.9        37.2         0.1        100.0

    1.8          18.2        32.7        46.9         0.3        100.0

    2.3            9.7        15.4        72.5         0.1        100.0

    6.7          30.0        24.9        38.1         0.3        100.0

    0.7            8.0        27.9        63.3         0.0        100.0

  10.9          21.2        25.5        41.7         0.7        100.0

    3.1          17.5        31.8        47.3         0.3        100.0

 

 

  37.3          20.2          4.0        37.9         0.6        100.0

  29.5          14.2        14.9        41.2         0.2        100.0

  32.0            6.9        11.0        49.1         1.0        100.0

 

 

  36.8          35.7        10.2        17.2         0.1        100.0

  24.1          32.4        12.9        30.5         0.1        100.0

  47.6          13.2          5.6        33.7         0.0        100.0

  62.7          15.8          8.1        13.1         0.3        100.0

ppm: Parts per million

 

 

 

Table V

 

Simplified classification of Goiter

_____________________________________________

Grade  O :                   No palpable or visible Goiter.

______________________________________________________________________

Grade  1  :                  A mass  in  the  neck  that  is  consistent   with   an enlarged

                                   thyroid  that is  palpable  but   not visible (PNV) when the neck is in

                                   the  normal  position. It moves upward  in  the  neck   as  the

                                   subject    swallows.    Nodular  alteration(s)   can  occur even

                                   when the thyroid is not visibly enlarged.

 

Grade 2 :                 A swelling in the neck that  is  visible  (V) when the neck is in  a

                                  normal   position     and    is   consistent   with   an enlarged

                                  thyroid    when   the  neck  is   palpated.

________________________________________________________________________

 

 

 

Table VI

 

 

Epidemiological criteria for assessing the  severity  of  IDD based on the prevalence of Goiter in  school  age     children

_________________________________________________________

Prevalence of Goiter      Mild IDD         Moderate IDD       Severe IDD

_________________________________________________________

        TGR                       5.0-19.9%       20.0-29.9%            >30.0%

 

 

 

Table.  VII

 

Epidemiological criteria for assessing severity of  IDD based on median urinary

              iodine levels.

             ________________________________________

              Median value                       Severity of IDD

             ________________________________________

               < 20                                   Severe IDD

               20-49                                 Moderate IDD

               50-99                                 Mild IDD

               > 100                                 No deficiency

            ________________________________________

 

 

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