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The Journal of Clinical Endocrinology & Metabolism Vol. 83, No. 10 3755-3756
Copyright © 1998 by The Endocrine Society


Letters to the Editor

A Never-Ending Story of an Insufficient Iodine Status Without Mandatory Iodization of Foods?—A German Experiencec

Thomas Remer and Annette Neubert

Forschungsinstitut für Kinderernährung (Research Institute of Child Nutrition), Heinstück 11, 44225 Dortmund, Germany

The most widely used biochemical indicator for the assessment of iodine status is urinary iodine excretion (1, 2). Endemic goiter and low urinary iodine excretion levels have been scientifically documented for decades and are still present in Europe (3, 4). In Germany (and similarly in a number of other European countries) the major cause of this is the legislation on micronutrient fortification, which still does not allow or lay down the mandatory iodization of foods.

After it became clear that increasing the iodine content of iodized table salt from 5 to 20 mg/kg, enforced in 1981, only marginally improved the iodine status of the German population, additional legislative measures were undertaken. In 1989 it became legal to add iodized salt to industrially processed foods and to canteen meals; then in late 1991 the use of iodized salt in the pickling of meat and sausages was legalized, and finally a decree issued in December 1993 superseded the previous law where the use of iodized salt in the food processing had to be separately labelled and declared by all food producers.

To evaluate the effects of the above stages in the German "iodine deficiency prophylaxis programme" urinary iodine excretion rates were measured along with body weight and body height in 541 healthy children aged 3–18 yr from 1986–1997. All the children studied were participants in the DONALD (Dortmund Nutritional and Anthropometrical Longitudinally Designed) study, a prospective mixed longitudinal cohort study on nutrition, growth, and metabolism from birth to maturity. Urinary 24-h iodine excretion rates were related to individual body surface area (standardized to adult body surface area of 1.73 m2) to fully control for the age dependency of urinary iodine output during growth (5). External iodine contaminations of the 24-h urine samples were avoided (6). Each child collected one 24-h urine sample per year and contributed between 1 and 12 specimens to the total number of 2404 urine samples analyzed during the 12 year observation period. As shown in Fig. 1Go, the very low urinary iodine excretion level seen in 1986 was still present in 1992 (median output: 66 and 71 µg/day/1.73 m2, respectively corresponding to a median urinary iodine concentration of 68 and 67 µg/L, respectively). Thereafter, a steady increase occurred, and a median output of 99 µg iodine/day/1.73 m2 was reached in 1997 (corresponding to a still insufficient (4) median urinary iodine concentration of 95 µg/L). Cross-sectional statistical analysis (ANOVA) on the logarithmic transformed data followed by t-tests revealed a significant (P < 0.05) rise in urinary iodine excretion (µg/day/1.73m2) one year after the third legislative measure (i.e. from 1993 to 1994) but no significant (P > 0.1) increase one year after the first (from 1989 to 1990) or the second (from 1991 to 1992) measure.



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Figure 1. Urinary iodine excretion from 1986 to 1997 in a group of 541 German children (values shown are median, 25th and 75th percentiles). Time points of specific legislative measures are indicated by arrows. Figures in parentheses show the number of subjects (24-h urine samples) investigated at the respective year.

 
Thus, the removal of the restricting decree on separate labelling of food containing iodized salt (in 1993) exerted the strongest "in vivo" impact on the iodine status in this exemplary group of German children in the last 12 years. The fact that only parts of food industry, bakeries, butchers and canteens no longer refuse to use iodized salt is probably the main reason why the median urinary iodine excretion is still markedly below 150 µg/day/1.73m2, i.e. below the recommended daily iodine intake of 150 µg/day (7). Thus, this kind of "liberal" handling of the iodization of foods is obviously not sufficient to adequately improve iodine status. It appears that, without appropriate legislative measures to enforce universal salt iodization as recommended by the WHO (7), the insufficient iodine status in Germany and in other European countries (4) could become a never-ending story.

We acknowledge support by grants from the Forum Schilddrüse e. V.

Footnotes

Address correspondence to: Thomas Remer, Research Institute of Child Nutrition, Heinstück 11, Dortmund, Germany 44225.

Received July 24, 1998.

References

  1. Rendl J, Bier D, Groh T, Reiners C. 1998 Rapid urinary iodide test. J Clin Endocrinol Metab. 83:1007–1012.[Abstract/Free Full Text]
  2. Smyth PP, Hetherton AM, Smith DF, Radcliff M, O’Herlihy C. 1997 Maternal iodine status and thyroid volume during pregnancy: correlation with neonatal iodine intake. J Clin Endocrinol Metab. 82:2840–2843.[Abstract/Free Full Text]
  3. Hampel R, Gordalla A, Zöllner H, et al. 1997 Alimentäre Jodaufnahme bei Jugendlichen in Mecklenburg-Vorpommern zwischen 1993 und 1996 gestiegen. Z Ernährungswiss. 36:151–154.[CrossRef][Medline]
  4. Delange F, Benker G, Caron Ph, et al. 1997 Thyroid volume and urinary iodine in European schoolchildren: standardization of values for the assessment of iodine deficiency. Eur J Endocrinol. 136:180–187.[Abstract/Free Full Text]
  5. Remer T, Manz F. 1994 The inadequacy of the urinary iodine-creatinine ratio for the assessment of iodine status during infancy, childhood, and adolescence. J Trace Elem Electrolytes Health Dis. 8:217–219.[Medline]
  6. Neubert A, Remer T. 1996 Measurement of urinary iodine concentration. Lancet. 347:1414–1415.
  7. WHO/UNICEF/ICCIDD. 1997 Recommended iodine levels in salt and guidelines for monitoring their adequacy and effectiveness. IDD Newsletter. 13:10–11.




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