ESPE Abstracts

The differences between people in degree of obesity within a given population are attributable to a combination of differences in their genomes and in what they have been exposed to in the environment. The heritability, which indicates the proportion of the phenotypic variance that is due to the genomic variation within this given population, is often estimated to a broad range of 40-80%, dependent on methods used (family versus twin studies), and is often interpreted as defining the limits of environmental influences (20-60%). However, this is an important misunderstanding, best exemplified by the rapidly rise of the prevalence of obesity within most populations around the world, which must be due to changes in environmental exposures (i.e. 100% environmental, barring likely minor contributions from assortative mating and migration). The essential questions are which specific environmental exposures induce obesity in the individuals, which have changed over time and thereby induced the obesity pandemic, and which are realistically modifiable. Whereas eating food in excess of the needs can enlarge the fat depots, it does not seem to produce the obesity phenotype, characterized by its resistance to being reduced, so it is necessary to search for other causes and mechanisms of obesity development. The energy value of the stored fat in obesity is always a tiny fraction (usually <1%) of the total energy consumed during obesity development, which is easily trapped from the food. Since obesity development is accompanied by excessively growing and energy consuming lean body mass, persisting food abundance can be seen as a permissive condition for obesity development. When this condition is met, it appears that exposure to a variety of psychosocial disadvantages and adversities along the life course within and between families increases the likelihood of obesity development, even at the pre-conceptional stage. Other environmental factors may play a role, e.g. parental smoking before birth, and many have been proposed, but there remains much uncertainty about the causal roles, both at the individual and population levels, and also about the often presumed interaction with the specific genetic predisposition.