gms | German Medical Science

50. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie (gmds)
12. Jahrestagung der Deutschen Arbeitsgemeinschaft für Epidemiologie (dae)

Deutsche Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie
Deutsche Arbeitsgemeinschaft für Epidemiologie

12. bis 15.09.2005, Freiburg im Breisgau

What are the Causes of the Obesity Epidemic?

Meeting Abstract

Suche in Medline nach

  • Thorkild I. A. Sorensen - Copenhagen University Hospital, Copenhagen

Deutsche Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie. Deutsche Arbeitsgemeinschaft für Epidemiologie. 50. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie (gmds), 12. Jahrestagung der Deutschen Arbeitsgemeinschaft für Epidemiologie. Freiburg im Breisgau, 12.-15.09.2005. Düsseldorf, Köln: German Medical Science; 2005. Doc05gmds664

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/gmds2005/05gmds157.shtml

Veröffentlicht: 8. September 2005

© 2005 Sorensen.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

An epidemic is defined as occurrence of a disease greatly in excess of expectation within a particular population. The term ‘the obesity epidemic’ refers to the rising prevalence of obesity (BMI≥30) or overweight (BMI≥25) in most populations of the world. The prevailing interpretation of its causes is that the societies have created a more and more ‘obesigenic’ environment, because the genetic causes, as the only alternative explanation, cannot change so rapidly. The ‘obesigenic’ environment is assumed to be continuous exposure to living conditions that eventually creates a positive energy balance of the body by increasing energy intake and reducing energy expenditure by physical activity, leading to deposition of the surplus of energy as fat in the adipose tissue. It is generally assumed that those who become obese in this environment are those susceptible to the environmental changes due to their genetic predisposition. If this paradigm is true, meaning that it is an exclusive and exhaustive interpretation of the epidemic, then the public health challenges to combat the epidemic is huge and perhaps impossible unless fundamental dimensions of the societies - through political and cultural (r)evolutions - are transformed. There is obviously a need to review the components of the paradigm of the obesity epidemic to see which are based on observational or experimental scientific evidence and which are implicit assumptions. There are several elements of circular reasoning in the paradigm, but it seems as if the main missing link is the lack of support to the assumption that the changes of the ‘obesigenic’ environment, as conceived, provides an adequate explanation of the development of the epidemic. Very few attempts to generate this evidence have apparently been undertaken, and when done they do not provide an unambiguous support. Studies that can address the development of the epidemic in time and space in sufficient detail suggest that an environmental conditioning may take place very early in life, adding to the genetic susceptibility. If this is true, it will pave the way for a preventable target in a limited time window at an age, where preventive actions are commonly accepted, such as vaccinations.