Horm Metab Res 2007; 39(9): 702
DOI: 10.1055/s-2007-985396
Letter to the Editor

© Georg Thieme Verlag KG Stuttgart · New York

Increased Prevalence of Thyroid Disease in Emigrants of the Former Soviet Union: Is the Hypothalamus-Pituitary-Adrenal (HPA) Axis Involved?

A. Schuppenies 1 , S. Fischer 1 , S. R. Bornstein 1 , W. Korenblum 1
  • 1Endocrinology, Diabetes and Metabolism, Department of Medicine, Carl Gustav Carus, University of Dresden, Dresden, Germany
Further Information

Publication History

received 16.03.2007

accepted 16.03.2007

Publication Date:
10 September 2007 (online)

Increasing evidence suggests a correlation between stress, depression, and thyroid disease [1] [2] [3]. Considering the worldwide challenge of metabolic diseases, the need for global prevention programs has become evident [4] [5] [6] [7]. Tsatsoulis has discussed the hypothesis that stress may lead to thyroid autoimmunity by shifting the T helper 1 to T helper 2 balance to an overexpression of T helper 2 cells via the hypothalamus-pituitary-adrenal axis in susceptible individuals [1]. We have found an increased prevalence of thyroid disease in a group of emigrants from the former Soviet Union, with emigration known to be an important stress factor [8]. We compared the data from 1009 Jewish “quota” refugees that had mostly emigrated from major cities in the European part of the former Soviet Union and 209 German resettlers mostly from rural areas in the Asian part of the Soviet Union aged 18-79 years with the data from a German-born population (n=5054) at the same family practice in Düsseldorf.

The occurrence of thyroid disease (inflammatory, autoimmune, and endemic) accounted for 20.9% in the population of Jewish refugees compared to 19.3% in the German resettler population and 15.2% in German-born population. We compared these data with official statistics from the North Rhine-Westphalia region and found a prevalence of 14.8% for thyroid disease [5] [6] [7].

Females showed higher thyroid disease prevalence in all the three groups - about 20% higher in immigrant females (30.9% in Jewish and 28.2% in resettler populations) than in German-born females (24.2%). In male immigrants, the prevalence was about twice as high (8.8% and 7.1%, respectively) as in German-born males (4.6%). Unfortunately, there was no distinction between the types of thyroid disease, but the greatly increased prevalence in females suggests that there is a large proportion of autoimmune thyroid disease, which is known to be more common in females; and the hypothesis of altered balance in the HPA axis as a cause of autoimmune disease may indeed apply.

A much simpler explanation for the comparatively high prevalence of thyroid disease in immigrants could be the endemic lack of iodine in the places of origin, a situation that may well have been ameliorated in Germany by iodine substitution policy that began in the eighties. With this as a possible cause, immigrants would contract thyroid disease, experience stress through the disease and may therefore display an imbalance in HPA axis regulation, developing depression and other mood-related symptoms. Cause and effect may be hard to distinguish in this and other cases, but the HPA axis still plays a very apparent and major role.

References

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  • 9 Weilandt C, Huismann A, Joksimovic L, Klaes L, Toom S van den, Winkler J. Sonderbereicht im Rahmen der Gesundheitsuntersuchung Nordrhein-Westfahlen. Herausgeber: Ministerium für Frauen, Jugend, Familie und Gesundheit des Landes Nordrhein-Westfalen, Düsseldorf 2000
  • 10 Rommel A, Cosler D, Klaes L, Stolle I, Potthoff P, Klamert A, Reis U, Schroeder E. Gesundheitssurvey Nordrhein-Westfalen. Herausgabe und Vertrieb: Ministerium für Frauen, Jugend, Familie und Gesundheit NRW 2002
  • 11 Statistisches Bundesamt Deutschland .Die Gesundheitsberichtserstattung des Bundes. Wiesbaden 2006

Correspondence

S. R. BornsteinMD, PhD 

Director and Chair

Department of Medicine

Carl Gustav Carus

University of Dresden

Fetscherstrasse 74

01307 Dresden

Germany

Phone: +49/351/458 59 55

Fax: +49/351/458 63 98

Email: stefan.bornstein@uniklinikum-dresden.de

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