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EDITORIAL
Year : 2010  |  Volume : 54  |  Issue : 4  |  Page : 175-178  

Iodine deficiency disorders: A health policy and planning perspective


Professor, Senior Advisor and Epidemiologist, Department of Community Medicine, Armed Forces Medical College, Pune; Joint Editor, Indian Journal of Public Health, India

Date of Web Publication3-Mar-2011

Correspondence Address:
Atul Kotwal
Professor, Senior Advisor and Epidemiologist, Department of Community Medicine, Armed Forces Medical College, Pune; Joint Editor, Indian Journal of Public Health
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-557X.77255

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How to cite this article:
Kotwal A. Iodine deficiency disorders: A health policy and planning perspective. Indian J Public Health 2010;54:175-8

How to cite this URL:
Kotwal A. Iodine deficiency disorders: A health policy and planning perspective. Indian J Public Health [serial online] 2010 [cited 2019 Nov 16];54:175-8. Available from: http://www.ijph.in/text.asp?2010/54/4/175/77255

Health program planners and administrators take pride in the fact that many of the National Health Programs in our country are being implemented since several decades and considerable achievements have been made in our efforts to improve health standards such as life expectancy, child mortality, infant mortality, and maternal mortality. Nevertheless, problems abound, like malnutrition affecting a large proportion of children, an unacceptably high morbidity and mortality from emerging and re-emerging diseases, and pregnancy- and childbirth-related complications. [1] It is time we introspect why the outcomes and impact of our programs and interventions are not as per desired levels and to examine if there is a need to adopt a different approach in health planning? Various analyses have shown that a techno-centric, reductionist approach has been propagated at the cost of an eco-socio-epidemiological approach. In this context, an attempt has been made to suggest a way forward for the health programs by citing an example of one of the programs.

The increasing global emphasis on technological solutions to problems in public health has subordinated the role of socio-economic factors in health and disease in addition to a shift in prioritization of public health problems. This trend has serious implications for public health, not only because it leaves out many of the problems crying for attention but also because technology-oriented professionals create misconceptions about the nature of the problems and the required interventions without adequately examining or basing the program design on the evidence. Prevention is thus assumed to be a technological challenge or at best of health education and inputs outside the scope of medical intervention tend to be ignored. [2] While technologies are crucial and necessary for public health, to contribute meaningfully in determining priorities and assessing the impact of intervention, their choice has to be based on sound evidence to retain the essence of a scientific method. [3] In this connection, the on-going debate on the extent of iodine deficiency disorders (IDD), in the context of a national strategy for its control, offers a good example of why we need to strive for objectivity in the practice of science.

The early pioneers described an endemic goiter belt along the southern slopes of the Himalayas and mapped the areas with goiter and deaf-mutism in other regions, demonstrating moderate rates in coastal and hill areas. [4],[5] Both studies pointed to various causative factors and the complex etiology of goiter. However, later studies focused only on one causal factor: the low iodine levels. [6],[7] Iodization of edible salt, a measure initiated in the United States and other countries in the 1920s, was adopted. The Government of India instituted the National Goiter Control Program (NGCP) in 1962 with a strategy composed of surveys in suspected endemic areas, supply of iodized salt in endemic areas, prohibition of non-iodized salt in those areas, and resurvey after periodic intervals to assess the impact of this strategy.

The program however faltered on many counts and problems were identified in the 1980s. In some areas, availability of adequately iodized salt was poor; in others, people's acceptance in terms of buying and consuming iodized salt was low, which was attributed to its higher price. [8],[9],[10] A working group's recommendations for universal iodization in India ensured non-availability of cheaper, non-iodized salt. Giving time to expand production capacities, the year 1990 and then 1992 was set for universal iodization and the program was renamed as National Iodine Deficiency Disorders Control Program (NIDDCP). Thus, no serious attempt was made to understand the reasons for people's non-acceptance of iodized salt, whether poverty and the added cost, lack of information, or other factors. In contrast, production and supply of iodized salt were given over to the private sector in 1984, leading to an increase in retail price for the consumer and profits for private industry. [8],[11]

Areas other than the Himalayan/sub-Himalayan, which had earlier been identified as endemic for deaf-mutism and goiter, [5] were ignored by the NGCP until the late 1970s. Studies then rediscovered IDD in these regions, [12] providing an added rationale for universalization of iodized salt (USI). New endemic areas were identified as well, such as Delhi. [13] Issues of multicausality and the possible negative effects of excessive iodine intake [14] continued to be ignored. In 1997, a countrywide ban on the sale of non-iodized edible salt was promulgated by the central government. Citizens' groups, associations of small-scale salt producers, and traders protested against it. Public health scientists raised serious questions about the rationale of a universal ban. [8],[10],[15] The states of Kerala and Gujarat did not accept it at all, and the ban was only partial in West Bengal and Maharashtra. The ban was revoked by the central government in the year 2000. [16] In May 2005, a notification was issued by the central government proposing a ban that would be binding on all states and, despite the objections filed, this was formalized in November 2005. [17]

The latest WHO review [18] traces an increasing trend of global Total Goiter Prevalence (TGP) between 1993 and 2003 (estimating a 31.7% increase), but finds that 72 of the 126 countries have reached sufficiency in iodine intake (median UIE, Urinary Iodine Excretion >100 μg/l). Yet, the review provided an unqualified reaffirmation to the effectiveness of USI and the continuing need for its strengthening. Several possible explanations have been offered for this discrepancy, but these are at best partial, raising further questions. To elaborate on one of the issues, a time lag should mean a delayed decrease, so why an increase? If TGP declined from 1998 to 2003, a steep rise in TGP from 1993 to 1998 is implied, and if it actually occurred, what is the explanation? What do the limitations of goiter surveys, now being recognized, imply for interpretation of earlier studies [19] ?

Though various studies show a decline in TGP in the endemic areas in all regions, diverse regional patterns emerge in the high endemic areas with clustering of TGPs in a particular range in each region and the TGP range varying across regions even when they have reached similar median UIE levels or percentage households using iodized salt. Within each region, the expected correlation between TGP declines, UIE levels and household iodized salt levels are flouted so often that it cannot merely be "exceptions to the rule." A high proportion of populations are going into what have been labeled as "excessive iodine intakes" by WHO, along with growing evidence for escalating autoimmune thyroiditis and its association with USI, and studies are available on the possible link of increased iodine intake leading to increased hypothyroidism/ hyperthyroidism. Monitoring of possible side-effects of increased iodine intakes needs to be undertaken on an urgent and continuing basis. [19],[20] A review [12] found the benefits of iodization to be overrated due to (a) overestimation of the problem, (b) ignoring multicausality, and (c) flawed impact assessment studies. Probable negative health consequences identified were (a) hyperthyroidism, (b) hypothyroidism, and (c) interaction with other micronutrients.

The epidemiological studies of thyroid disorders suffer from various drawbacks and moreover comparison of results of epidemiological surveys carried out in various states, countries, and over a period of time within same community or country is often invalid. This is further compounded by different methodologies used to present the results and investigators' interpretation of classification criteria. The evidence from trials and other studies is conflicting as most of the studies showed only a marginal decrease in the prevalence of goiter despite the so-called USI. The reasons for the lack of effectiveness have never been considered for evaluating the program strategy. There is a definite lack of cohort studies at present and as with other aspects, the assessment of intervention, i.e. iodized salt/oil also suffers from various drawbacks. [20] Continuing TGPs above 5% in areas with high UIE indicates not only the limits of iodization as a measure, but also that it can cause a different pattern of thyroid pathology in the population. Human iodine levels in several populations have increased above optimal. This can seriously affect quality of life and increase comorbidities, especially in young women. On reviewing the data from an ecological perspective, conditions of stable thyroid balance and imbalance appear as a pattern, the diverse processes determining prevalence of thyroid disorders suggesting an "ecological balance hypothesis". [19]

These reviews show that wherever endemic IDD does exist, it is a problem with socio-economic, developmental and ecological causes. Rarely has it been tackled successfully through iodine supplementation alone. Iodine deficiency of soil is related to flooding, deforestation, and soil degradation. Changes in dietary patterns could be significant factors. Changing exposure to bacterial flora could be another issue. The lack of food exchanges is also important in the causation of endemic goiter. These factors could be interacting at different levels in various regions and so local factors of significance need to be identified. A program to combat iodine deficiency should essentially tackle these issues for a long-term and sustainable solution rather than looking at a single intervention of iodized salt alone. Development and ecology thus should be the key areas of focus to reduce IDD. The problem of goitrogens in food, water, and synthetic chemicals and the role of polluted water need to be understood and taken care of rather than just pushing iodized salt as a panacea for the prevention and control of IDD.

Further, an ecological basis used for understanding the dynamics of the iodine-thyroid axis explains the frequent discrepancies between iodine intake, urinary iodine, hormone levels and goiters, as well as the observed global increase in hyperthyroidism and hypothyroidism with an increase in intake of iodine. The ethics of public health demands that the possible negative consequences, of interfering with iron metabolism and thereby enhancing anemia and the increase in goiter due to excess iodine, need to be investigated under diverse conditions. [2],[12],[19] Thus, evidence from scientific, systematic reviews provides enough basis to question the current dominant paradigm and enough evidence to start a fresh debate on: iodine as the sole factor in causality; magnitude of the problem as a major public health problem universally; effectiveness of universal iodization of salt as a measure that leads to decreasing goiter and other IDD by itself; and possible negative impacts on health itself like increase in hyperthyroidism, goiter, hypothyroidism, and interaction with other minerals like iron.

Based on the issues discussed above, suggestions have been made for developing a more epidemiologically and ecologically appropriate program approach, one that leaves people with choices, relies on community participation, and creation of facilitatory conditions. Whether international and/or the Indian public health policymakers will be willing to re-examine the evidence before them, be transparent in their decision making, and reform the conventional approach remain to be seen. But ecological and social perspectives have gained ground within public health in recent years, and so the struggle among paradigms may yet yield unexpected results. Based on the eco-social epidemiological understanding, the rational approach may be to develop a differential strategy for regions characterized by threshold levels and trends, as outlined by systematic reviews. [19],[20]

To summarize, the problem of IDDs has increased in many parts of the world [18] and the use of iodization as a strategy can at best claim to prevent further increase than present prevalence. [2],[12],[19] Thus, an IDD control program has to balance between preventing the ill-effects due to iodine deficiency and aggravation of other forms of hypothyroidism or hyperthyroidism which have been ignored until now. Multi-causality and regional diversity requires a range of approaches rather than a universal mono-solution.

As the adequacy of measures for the prevention and control of any disease depends upon the extent of knowledge at a point of time about its etiology and pathogenesis, appropriate conceptualization of its complexity, the availability of an effective intervention, implementation and subsequent evaluation and feedback/review of the program, we the acolytes of evidence-based medicine must take steps to prevent our medical successors, using the long lens of history, from judging us as harshly as we might judge the early history of prevention and control of IDDs.


   Acknowledgement Top


The author acknowledges Dr Ritu Priya, Professor and Dr Imrana Qadeer, Retired Professor of Centre for Social Medicine and Community Health, School of Social Sciences, Jawaharlal Nehru University, New Delhi for their critical inputs in the editorial.

 
   References Top

1.Eleventh FY Plan for the Health and Family Welfare and AYUSH (2007-2012). Vol 2, Chapter 3, New Delhi: Oxford University Press; 2008. p. 74-144.  Back to cited text no. 1
    
2.Qadeer I. Continuities and Discontinuities in Public Health: The Indian Experience, In: Amiya Kumar Bagchi and Krishna Soman ed: Debates in Public Health in India, New Delhi: Tulika Books; 2005. p. 79-96.  Back to cited text no. 2
    
3.Qadeer I, Priya R, Kotwal A. Research Base for Planning Control of Iodine-Deficiency Diseases in India: Is There a Bottom Line? eSocialSciences. Available from: http://www.esocialsciences.com /Articles/ display Articles.asp?Article_ID=268. [last cited in 2005].  Back to cited text no. 3
    
4.McCarrison R. Observations on endemic goitre in the Chitral and Gilgit valleys. Lancet 1906;1:1110.  Back to cited text no. 4
    
5.Stott H, Bhatia BB, Lal RS, Rai KC. The distribution and cause of endemic goitre in the United Provinces. Indian J Med Res 1930;22:1059-85.  Back to cited text no. 5
    
6.Ramalingaswami V, Subramanian TA, Deo MG. The aetiology of Himalayan endemic goiter. Lancet 1961;15:791-4.  Back to cited text no. 6
    
7.Sooch SS, Ramalingaswami V. Preliminary report of an experiment in the Kangra Valley for the prevention of Himalayan endemic goiter with iodized salt. Bull World Health Organ 1965;32:299-315.  Back to cited text no. 7
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8.Jayarao KS. "Ta-ta" to common salt or vice-versa? Medico Friend Circ Bull 1989;150:1-12.  Back to cited text no. 8
    
9.WHO Regional Office for South East Asia. Iodine Deficiency Disorders in South-East Asia. New Delhi, 1985.  Back to cited text no. 9
    
10.Pandav CS, Kochupillai N, Karmarkar MG, Nath LM. Iodine deficiency disorders in India: Review of control measures. Indian Pediatr 1986;23:325-9.  Back to cited text no. 10
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11.Pandav CS, Kochupillai N, Karmarkar MG, Nath LM. Endemic goiter: Why the apathy? Review of the National Goiter Control Program. Econ Polit Wkly 1986;21:1121-7.  Back to cited text no. 11
    
12.Kotwal A, Priya R, Qadeer I. Goiter and other Iodine Deficiency Disorders: A Systematic Review of Epidemiological Studies to Deconstruct the Complex Web. Arch Med Res 2007;38:1-14.   Back to cited text no. 12
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13.Pandav CS, Mallik A, Anand K, Pandav S, Karmarkar MG. Prevalence of iodine deficiency disorders among school children of Delhi. Natl Med J India 1997;10:112-4.  Back to cited text no. 13
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14.Stanbury JB, Ermans AE, Todd C, Oken E, Tonglet R, Vidor G, et al. Iodine-induced hyperthyroidism: Occurrence and epidemiology. Thyroid 1998;8:83-100.  Back to cited text no. 14
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15.Aravindan KP. National Policy for Universal Salt Iodization: A Critique. Trichur, Kerala, India: Kerala Sastra Sahitya Parishad; 1989. p. 1-21.  Back to cited text no. 15
    
16.Government of India. Ministry of Health and Family Welfare (Department of Health), Notification on Amendment to the PFA Rules, 1955. Gazette of India, Extraordinary, Sept. 13, Pt. II, Sect. 3, 2000.  Back to cited text no. 16
    
17.Government of India. Ministry of Health and Family Welfare (Department of Health), Notification on Amendment to the PFA Rules, 1955. Gazette of India, Extraordinary, No. 226, May 27, 2005.  Back to cited text no. 17
    
18.Iodine Status Worldwide: WHO Global database on Iodine deficiency. Department of Nutrition for Health and Development, World Health Organization. 2004. http://www.whqlibdoc-who.int/publications/2004/9241592001.pdf. [last accessed on 2006 Jan].  Back to cited text no. 18
    
19.Priya R, Kotwal A, Qadeer I. Towards an Eco-Social Epidemiology Approach to Goitre and Other Iodine Deficiency Disorders: A Review of India′s Technocratic Program for Universal Iodisation of Salt. Int J Health Serv 2009;39:343-62.  Back to cited text no. 19
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20.Kotwal A, Priya R, Qadeer I, Kotwal J. Goitre And Other Iodine Deficiency Disorders: Entire Issue Revisited. In: Lt Gen (Retd) Sachdev YR, editor. Text Book of Endocrinology. New Delhi: Jaypee Publishers; 2008  Back to cited text no. 20
    



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