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Goiter and Other Iodine Deficiency Disorders: A Systematic Review of Epidemiological Studies to Deconstruct the Complex Web
Archives of Medical Research 38 (2007) 586e587
LETTER TO THE EDITOR
Goiter and Other Iodine Deficiency Disorders: A Systematic Review of Epidemiological Studies to Deconstruct the Complex Web
To the Editor: The Review Article by Kotwal et al. (1) may perhaps serve as a useful reminder of the difficulty that arises from the exclusive use of epidemiological studies to develop a paradigm. Moreover, when adding population studies of efforts to tackle the problem of iodine deficiency, the case soon becomes compounded by the fact that measurements of goiter perform poorly in evaluation (2). Approaching the IDD paradigm from the etiology and causation of goiter is inadequate. It has been known for a long time that severe iodine deficiency in a population guarantees that some individuals will exhibit the typical features of endemic cretinism (3). In an effort to address the question whether cretinism appears in a community as an all-or-nothing event arising from severe iodine deficiency, or whether there are lesser degrees of neurological damage to individuals from iodine deficiency in the same population, Stanbury brought the leading scientists together at the Franklin Institute of Philadelphia in 1993 and gave the published conference proceedings the telling title of ‘‘The Damaged Brain of Iodine Deficiency’’ (4). And in one of his final contributions to science, the most eminent ever Indian medical scientist Ramalingaswami in a keynote speech at the 8th World Salt Symposium declared: ‘‘The realization has finally dawned that iodine deficiency in the population also affects the intellectual performance of those members who have no apparent clinical symptoms. This revealed the true nature of the problem: in populations with iodine deficiency, all are affected, even if the impact on the individual is not perceived or clinically demonstrable’’ (5). In dismissing the evidence for benefits of iodized salt, the authors apparently overlooked some of the more recent publications from experimental and epidemiological studies by Zhao et al. (6), Jooste et al. (7) and others that show an immediate effect on iodine status but a trailing impact on reduced goiter prevalence especially if the additional iodine intake from iodized salt consumption falters or fluctuates. Finally, it is somewhat surprising that in their paragraph on harmful effects of dietary iodine, the authors cite a study
by the group of investigators led by Laurberg in Denmark, a country where the solution of the iodine deficiency problem in the population is being approached in a most careful, minimalist manner just to evade the increase in hyperthyroidism incidence that is bound to occur with mandatory salt iodization (8,9). In a recent editorial in the New England Journal of Medicine, Utiger commented: ‘‘Overall, the small risks of chronic iodine excess are outweighed by the substantial hazards of iodine deficiency, which is still widespread’’ (10). Goiter and cretinism have plagued humankind for millenniums. It has taken medical scientists more than a century to understand that iodine deficiency is the underlying cause and it took at least another 50 years for the world to arrive at an apex of action to reach sustainable elimination of IDD (Ramalingaswami op cit). In conclusion of their review, Kotwal and co-authors suggest ‘‘a fresh debate’’. It is questionable, however, whether a new debate leads to a constructive outcome when the current dominant paradigm is not recognized.
References 1. 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;38:1e14. 2. Assessment of Iodine Deficiency Disorders and Monitoring their Elimination: A Guide for Programme Managers (second edition). Geneva: ICCIDD, UNICEF, WHO; 2001. p. 40. 3. Querido A. Endemic cretinism e a continuous personal educational experience during 10 years. Postgrad Med J 1975;51:591e599. 4. Stanbury J. The Damaged Brain of Iodine Deficiency. New York, NY: Cognizant Communication Corporation; 1994. 5. Ramalingaswami V. The public health imperative of permanent elimination of iodine deficiency. In: Geertman R, ed. 8th World Salt Symposium. Amsterdam, The Netherlands: Elsevier; 2000. pp. 3e11. 6. Zhao J, Fujie X, Zhang Q, Shang L, Xu A, Goa Y, et al. Randomized clinical trial comparing different iodine interventions in school children. Publ Health Nutr 1999;2:173e178. 7. Jooste PL, Weight MJ, Lombard CJ. Short-term effectiveness of mandatory iodization of table salt, at an elevated iodine concentration, on the iodine and goiter status of schoolchildren with endemic goiter. Am J Clin Nutr 2000;71:75e80.
0188-4409/07 $esee front matter. Copyright Ó 2007 IMSS. Published by Elsevier Inc. doi: 10.1016/j.arcmed.2007.04.001
Letter to the Editor / Archives of Medical Research 38 (2007) 586e587 8. Pedersen IB, Knudsen N, Joergensen T, Perrild H, Ovesen L, Laurberg P. Large differences in incidences of overt hyper- and hypothyroidism associated with a small difference in iodine intake: a prospective comparative register-based population study. J Clin Endocrinol Metab 2002;87:4462e4469. 9. Vejbjerg P, Knudsen N, Perrild H, Carle A, Laurberg P, Pedersen IB, et al. Effect of a mandatory iodization program on thyroid gland volume based on individuals’ age, gender, and preceding severity of dietary iodine deficiency: a prospective, population-based study. J Clin Endocrinol Metab 2007;92:1397e1401. 10. Utiger RD. Iodine nutrition—More is better. N Engl J Med 2006;354: 2819e2821.
587
FRITS VAN DER HAAR, PhD Emory University Rollins School of Public Health Atlanta, Georgia Address reprint requests to: Frits Van Der Haar, PhD Emory University Rollins School of Public Health 1520 Clifton Rd, N.E. Ste. 238, Atlanta, GA 30322 E-mail: [email protected] Received for publication March 5, 2007; accepted April 9, 2007 (ARCMED-D-07-00100).
LETTER TO THE EDITOR
Goiter and Other Iodine Deficiency Disorders: A Systematic Review of Epidemiological Studies to Deconstruct the Complex Web
To the Editor: The Review Article by Kotwal et al. (1) may perhaps serve as a useful reminder of the difficulty that arises from the exclusive use of epidemiological studies to develop a paradigm. Moreover, when adding population studies of efforts to tackle the problem of iodine deficiency, the case soon becomes compounded by the fact that measurements of goiter perform poorly in evaluation (2). Approaching the IDD paradigm from the etiology and causation of goiter is inadequate. It has been known for a long time that severe iodine deficiency in a population guarantees that some individuals will exhibit the typical features of endemic cretinism (3). In an effort to address the question whether cretinism appears in a community as an all-or-nothing event arising from severe iodine deficiency, or whether there are lesser degrees of neurological damage to individuals from iodine deficiency in the same population, Stanbury brought the leading scientists together at the Franklin Institute of Philadelphia in 1993 and gave the published conference proceedings the telling title of ‘‘The Damaged Brain of Iodine Deficiency’’ (4). And in one of his final contributions to science, the most eminent ever Indian medical scientist Ramalingaswami in a keynote speech at the 8th World Salt Symposium declared: ‘‘The realization has finally dawned that iodine deficiency in the population also affects the intellectual performance of those members who have no apparent clinical symptoms. This revealed the true nature of the problem: in populations with iodine deficiency, all are affected, even if the impact on the individual is not perceived or clinically demonstrable’’ (5). In dismissing the evidence for benefits of iodized salt, the authors apparently overlooked some of the more recent publications from experimental and epidemiological studies by Zhao et al. (6), Jooste et al. (7) and others that show an immediate effect on iodine status but a trailing impact on reduced goiter prevalence especially if the additional iodine intake from iodized salt consumption falters or fluctuates. Finally, it is somewhat surprising that in their paragraph on harmful effects of dietary iodine, the authors cite a study
by the group of investigators led by Laurberg in Denmark, a country where the solution of the iodine deficiency problem in the population is being approached in a most careful, minimalist manner just to evade the increase in hyperthyroidism incidence that is bound to occur with mandatory salt iodization (8,9). In a recent editorial in the New England Journal of Medicine, Utiger commented: ‘‘Overall, the small risks of chronic iodine excess are outweighed by the substantial hazards of iodine deficiency, which is still widespread’’ (10). Goiter and cretinism have plagued humankind for millenniums. It has taken medical scientists more than a century to understand that iodine deficiency is the underlying cause and it took at least another 50 years for the world to arrive at an apex of action to reach sustainable elimination of IDD (Ramalingaswami op cit). In conclusion of their review, Kotwal and co-authors suggest ‘‘a fresh debate’’. It is questionable, however, whether a new debate leads to a constructive outcome when the current dominant paradigm is not recognized.
References 1. 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;38:1e14. 2. Assessment of Iodine Deficiency Disorders and Monitoring their Elimination: A Guide for Programme Managers (second edition). Geneva: ICCIDD, UNICEF, WHO; 2001. p. 40. 3. Querido A. Endemic cretinism e a continuous personal educational experience during 10 years. Postgrad Med J 1975;51:591e599. 4. Stanbury J. The Damaged Brain of Iodine Deficiency. New York, NY: Cognizant Communication Corporation; 1994. 5. Ramalingaswami V. The public health imperative of permanent elimination of iodine deficiency. In: Geertman R, ed. 8th World Salt Symposium. Amsterdam, The Netherlands: Elsevier; 2000. pp. 3e11. 6. Zhao J, Fujie X, Zhang Q, Shang L, Xu A, Goa Y, et al. Randomized clinical trial comparing different iodine interventions in school children. Publ Health Nutr 1999;2:173e178. 7. Jooste PL, Weight MJ, Lombard CJ. Short-term effectiveness of mandatory iodization of table salt, at an elevated iodine concentration, on the iodine and goiter status of schoolchildren with endemic goiter. Am J Clin Nutr 2000;71:75e80.
0188-4409/07 $esee front matter. Copyright Ó 2007 IMSS. Published by Elsevier Inc. doi: 10.1016/j.arcmed.2007.04.001
Letter to the Editor / Archives of Medical Research 38 (2007) 586e587 8. Pedersen IB, Knudsen N, Joergensen T, Perrild H, Ovesen L, Laurberg P. Large differences in incidences of overt hyper- and hypothyroidism associated with a small difference in iodine intake: a prospective comparative register-based population study. J Clin Endocrinol Metab 2002;87:4462e4469. 9. Vejbjerg P, Knudsen N, Perrild H, Carle A, Laurberg P, Pedersen IB, et al. Effect of a mandatory iodization program on thyroid gland volume based on individuals’ age, gender, and preceding severity of dietary iodine deficiency: a prospective, population-based study. J Clin Endocrinol Metab 2007;92:1397e1401. 10. Utiger RD. Iodine nutrition—More is better. N Engl J Med 2006;354: 2819e2821.
587
FRITS VAN DER HAAR, PhD Emory University Rollins School of Public Health Atlanta, Georgia Address reprint requests to: Frits Van Der Haar, PhD Emory University Rollins School of Public Health 1520 Clifton Rd, N.E. Ste. 238, Atlanta, GA 30322 E-mail: [email protected] Received for publication March 5, 2007; accepted April 9, 2007 (ARCMED-D-07-00100).