Abstract
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Proceedings of the Nutrition Society |
| Vol/bind | 68 |
| Udgave nummer | 1 |
| Sider (fra-til) | 43-54 |
| Antal sider | 11 |
| ISSN | 0029-6651 |
| DOI | |
| Status | Udgivet - 2009 |
Bibliografisk note
Keywords: Adipose Tissue; Adolescent; Basal Metabolism; Child; Diabetes Mellitus; Diet; Eating; Energy Intake; Energy Metabolism; Environment; Exercise; Female; Genetic Predisposition to Disease; Homeostasis; Humans; Infant, Low Birth Weight; Infant, Newborn; Male; Models, Theoretical; Obesity; Thermodynamics; Time Factors; Weight Gain; Young AdultAdgang til dokumentet
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Conference on "Multidisciplinary approaches to nutritional problems". Symposium on "Diabetes and health". Challenges in the study of causation of obesity. / Sørensen, Thorkild I A.
I: Proceedings of the Nutrition Society, Bind 68, Nr. 1, 2009, s. 43-54.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - Conference on "Multidisciplinary approaches to nutritional problems". Symposium on "Diabetes and health". Challenges in the study of causation of obesity
AU - Sørensen, Thorkild I A
N1 - Keywords: Adipose Tissue; Adolescent; Basal Metabolism; Child; Diabetes Mellitus; Diet; Eating; Energy Intake; Energy Metabolism; Environment; Exercise; Female; Genetic Predisposition to Disease; Homeostasis; Humans; Infant, Low Birth Weight; Infant, Newborn; Male; Models, Theoretical; Obesity; Thermodynamics; Time Factors; Weight Gain; Young Adult
PY - 2009
Y1 - 2009
N2 - Use of the energy balance equation for understanding the causation of obesity is discussed. Its basis on the thermodynamic laws is expressed in mathematical models for body-weight changes. Only a very small net energy surplus per time unit constitutes the energy deposition during weight gain, making measurements of its components difficult. The physical laws provide exact quantitative relationships between energy intake, energy expenditure and deposition of energy, but cannot disentangle the initiating and driving forces of the energy imbalance, which may also be an active storage of fat in adipose tissue. These and various other limitations of the energy balance model warrant cautiousness in using the model in studies of obesity causation. Weight gain may be self-promoting and mathematical feedback models allowing estimation of such effects show that they are realistic. Predisposition and susceptibility should be distinguished, and susceptibility as a modifiable predisposition, the genetic and environmental contribution to predisposition and its usefulness as targets for prevention and treatment are discussed. Current progress in unravelling genetic predisposition, the complex genetically-determined mechanisms, the slower progress in unravelling the environmental influences, the different nature of genetic and environmental influences, the possible pathways of environmental influences and the environmental influences as mediators of genetic effects are addressed. The evidence behind the prevailing concept of the 'obesogenic' environment is critically analysed. Finally, particular opportunities for the identification of the causes of the obesity epidemic by detailed analysis of an observed irregular development of the epidemic over long time periods are presented, and evidence for predisposition as a result of postnatal environmental influences is inferred from these studies.
AB - Use of the energy balance equation for understanding the causation of obesity is discussed. Its basis on the thermodynamic laws is expressed in mathematical models for body-weight changes. Only a very small net energy surplus per time unit constitutes the energy deposition during weight gain, making measurements of its components difficult. The physical laws provide exact quantitative relationships between energy intake, energy expenditure and deposition of energy, but cannot disentangle the initiating and driving forces of the energy imbalance, which may also be an active storage of fat in adipose tissue. These and various other limitations of the energy balance model warrant cautiousness in using the model in studies of obesity causation. Weight gain may be self-promoting and mathematical feedback models allowing estimation of such effects show that they are realistic. Predisposition and susceptibility should be distinguished, and susceptibility as a modifiable predisposition, the genetic and environmental contribution to predisposition and its usefulness as targets for prevention and treatment are discussed. Current progress in unravelling genetic predisposition, the complex genetically-determined mechanisms, the slower progress in unravelling the environmental influences, the different nature of genetic and environmental influences, the possible pathways of environmental influences and the environmental influences as mediators of genetic effects are addressed. The evidence behind the prevailing concept of the 'obesogenic' environment is critically analysed. Finally, particular opportunities for the identification of the causes of the obesity epidemic by detailed analysis of an observed irregular development of the epidemic over long time periods are presented, and evidence for predisposition as a result of postnatal environmental influences is inferred from these studies.
U2 - 10.1017/S0029665108008847
DO - 10.1017/S0029665108008847
M3 - Journal article
C2 - 19079823
VL - 68
SP - 43
EP - 54
JO - Proceedings of the Nutrition Society
JF - Proceedings of the Nutrition Society
SN - 0029-6651
IS - 1
ER -