Causes of juvenile obesity: Clues from epidemiology

T. I.A. Sørensen*, P. Myers, H. Møller, T. Jensen, W. Sippell, S. Guo, N. Skakkebæk, J. Huff, E. Lynge

*Corresponding author af dette arbejde

    Publikation: Bidrag til tidsskriftArtikelForskningpeer review


    A global epidemic of obesity is rapidly developing in children and adults, both in developed and developing countries. It is expected to create a huge public health problem in the future because of the conditions associated with obesity, both the immediate psychosocial and somatic problems and the longterm complications including glucose intolerance, type 2 diabetes, hypertension, hyperlipidaemia, and therefore an increased risk of cardiovascular diseases, increased risk of certain cancers and of gallstones, and eventually, excess mortality. It is commonly assumed that the causes of the epidemic is simple, namely both overeating and sedentary behavior, often in combination, and the preventive measures are all targeted to reverse this life style. When developed, obesity as such leads to overeating and physical inactivity for obvious reasons, but, unfortunately, it has not yet been possible to demonstrate that these behaviors precede the development of obesity. What are then the causes of obesity? Multiple family, twin and adoption studies leave no longer any doubt that obesity has a genetic predisposition that explains most if not all of the familial aggregation of obesity. Intensive search through the last 6 years has revealed some specific genes (e.g. leptin and the leptin receptor) that may cause obesity, but genetic variants that can account for the common obesity have not yet been identified. The development of obesity epidemic also shows that there in addition must be rapid environmental changes that may operate on the genetic background although clear gene-environment interaction (synergism/antagonism) has not yet been found. We have conducted detailed analyses of very large population-based Danish cohorts of boys in school age and young men examined as draftees, and we have have found that the obesity epidemic developed in two waves that appeared to be closely linked to birth cohorts and to be emerging already before school age: the first one during the 1940es and the second since mid 1960es. These findings strongly indicate that parallel preceding changes in the fetal or early childhood environment have played a role. To our great surprise, after having peaked among those born in the late 1980es, the prevalence of obesity in the young men is now rapidly declining again, further substantiating the role of rapidly altered environmental influences, the nature of which is unknown. Identification of the specific environmental factors may allow much more effective preventive measures to be taken in the future.

    Sider (fra-til)S171-S173
    TidsskriftAPMIS, Supplement
    Udgave nummer103
    StatusUdgivet - 31 jul. 2001


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