Adipositas - Ursachen, Folgeerkrankungen, Therapie 2008; 02(04): 181-186
DOI: 10.1055/s-0037-1618645
Adipositas und Lunge
Schattauer GmbH

Adipositas – Risikofaktor für die Asthmagenese im Kindes- und Jugendalter?

Obesity – risk factor for the development of asthma in children and adolescents?
J. Lecheler
1   CJD Asthmazentrum, Berchtesgaden
› Author Affiliations
Further Information

Publication History

Publication Date:
21 December 2017 (online)

Zusammenfassung

Die Häufigkeit von Adipositas steigt seit einer Generation bei Kindern und Jugendlichen ebenso an wie die Häufigkeit von Asthma bronchiale. Epidemiologische Untersuchungen lassen vermuten, dass es kausale Verknüpfungen zwischen diesen beiden Krankheitsbildern gibt. Die Einschränkungen der Lungenfunktion Adipöser lassen jedoch auch einen anderen Schluss zu: Verminderte Flussraten in der Spirometrie sind nur in Relation zur gleichsinnig verminderten Vitalkapazität zu verstehen und können, absolut genommen, missverständlich als Asthma interpretiert werden. Missverständnisse können auch durch falsche Bewertungen der subjektiv empfundenen Dyspnoe ausgelöst werden. Der pathologischer Ausfall in Hyperreagibilitätstests Adipöser andererseits ist auf funktionelle Veränderung der glatten Muskulatur in den Atemwegen zurückzuführen (“bronchial latching”). Diese adipositasinduzierte bronchiale Dysfunktion bedarf jedoch keiner antiinflammatorischen oder broncho- spasmolytischen Theapie. Körperliches Training und Gewichtsreduktion sind dagegen ein kausaler Behandlungsansatz. Ein passiveres Bewegungsverhalten im Kindes- und Jugendalter mit häufigem Medienkonsum führt nicht nur zur Zunahme von Adipositas, sondern trägt auch zur Asthma-Entwicklung bei. Adipositas und Asthma sind dabei unabhängig voneinander Folgen einer gemeinsamen Ursache, können sich später jedoch ungünstig verstärken.

Summary

For a generation, the incidence of obesity has been increasing in children and adolescents just like the incidence of asthma. Epidemiological studies have suggested causal associations between these two diseases. However, a different conclusion may be drawn from the impairments in lung function in obese patients: unless there are also reductions in vital capacity, reduced spirometric flow rates are, by themselves, not conclusive and can be misinterpreted as asthma. Misunderstandings can also be triggered by incorrect assessments of the subjective symptom of dyspnoea. On the other hand, the pathological deficit seen in hyperreactivity tests of obese patients is due to functional changes in smooth muscles of the respiratory tract (“bronchial latching”). This obesity-induced bronchial dysfunction does not however require any anti-inflammatory or bronchospasmolytic therapy. Instead, physical training and weight reduction are a causal approach to treatment. A more sedentary lifestyle in children and adolescents, with frequent media consumption, not only leads to an increase in obesity but also contributes to the development of asthma. Obesity and asthma are therefore independent consequences of one and the same cause but which can exacerbate each other later on.

 
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