The purpose was to investigate a possible levelling off in the obesity epidemic, by systematically reviewing literature and web-based sources. Eligible studies and data sources were required to have at least two measures of obesity prevalence since 1999. A literature and Internet search resulted in 52 studies from 25 different countries. The findings supported an overall levelling off of the epidemic in children and adolescents from Australia, Europe, Japan and the USA. In adults, stability was found in the USA, while increases were still observed in some European and Asian countries. Some evidence for heterogeneity in the obesity trends across socioeconomic status (SES) groups was found. The levelling off was less evident in the lower-SES groups. No obvious differences between genders were identified. We discussed potential explanations for a levelling off and the utility of investigating obesity trends to identify the driving forces behind the epidemic. It is important to emphasize that the levelling off is not tantamount to calling off the epidemic. Additionally, it is worthwhile to keep in mind that previous stable phases have been followed by further increases in the prevalence of obesity. Therefore, research into the causes, prevention and treatment of obesity should remain a priority.

In this systematic review, we aimed to collect together all previous twin and adoption studies on childhood and adolescent obesity up to the age of 18 years. Using several sources, we identified nine twin and five adoption studies; all of these studies had used relative weight as an indicator of obesity. Except the two twin studies from the Korean population, all studies represented Caucasian populations. In a meta-analysis of these twin studies, we found that genetic factors had a strong effect on the variation of body mass index (BMI) at all ages. The common environmental factors showed a substantial effect in mid-childhood, but this effect disappeared at adolescence. Adoption studies supported the role of family environment in childhood obesity as correlations were found between adoptees and adoptive parents; however, correlations were substantially stronger between parents and their biological offspring, further supporting the importance of genetic factors. In the future, more studies implementing genetic and environmental measures into twin models are needed as they allow estimation of the proportion of total genetic variation explained by candidate genes and analyses of gene-environment interactions. More studies of genetic architecture in non-Caucasian populations, of gene-environment interactions, and of body composition and body fat distribution are needed. IntroductionChildhood obesity is one of the major public health problems in the modern world. In the period [2003][2004][2005][2006], 32% of the US children were classified as obese or overweight, 1 and increasing trends in childhood obesity are seen all over the world. 2 These results are especially alarming as overweight children show a high risk of becoming obese adults. 3,4 Childhood is an important period of life for health interventions as health-related behaviors are just in formation, and it seems possible to intervene for preventing the development of obesity. 5 Thus, it is crucial to further understand the background mechanisms of childhood obesity to find even more effective measures to prevent it before it begins to produce more or less irreversible health damages.Both genetic and environmental factors will probably contribute to childhood obesity. 6 Family studies have shown that obesity runs in families, although more detailed twin, adoption and family studies have shown that genetic differences between individuals explain a major proportion of the within-population variation in body mass index (BMI, kg m À2 ) in adulthood. [7][8][9] It is probable that genetic factors have an important role in childhood obesity also, but their role may be different or they may result from other genes than those that operate in adulthood. 10 The environmental factors shared by family members, such as co-twins in twin studies, have shown only a slight effect on the variation of adult BMI. 7,8 However, they may have a more important role in childhood, where parents and their offspring live together and where siblings obviously have a much greater opportu...

Background and ObjectivesThere is no doubt that the dramatic worldwide increase in obesity prevalence is due to changes in environmental factors. However, twin and family studies suggest that genetic differences are responsible for the major part of the variation in adiposity within populations. Recent studies show that the genetic effects on body mass index (BMI) may be stronger when combined with presumed risk factors for obesity. We tested the hypothesis that the genetic variance of BMI has increased during the obesity epidemic.MethodsThe data comprised height and weight measurements of 1,474,065 Swedish conscripts at age 18–19 y born between 1951 and 1983. The data were linked to the Swedish Multi-Generation Register and the Swedish Twin Register from which 264,796 full-brother pairs, 1,736 monozygotic (MZ) and 1,961 dizygotic (DZ) twin pairs were identified. The twin pairs were analysed to identify the most parsimonious model for the genetic and environmental contribution to BMI variance. The full-brother pairs were subsequently divided into subgroups by year of birth to investigate trends in the genetic variance of BMI.ResultsThe twin analysis showed that BMI variation could be explained by additive genetic and environmental factors not shared by co-twins. On the basis of the analyses of the full-siblings, the additive genetic variance of BMI increased from 4.3 [95% CI 4.04–4.53] to 7.9 [95% CI 7.28–8.54] within the study period, as did the unique environmental variance, which increased from 1.4 [95% CI 1.32–1.48] to 2.0 [95% CI 1.89–2.22]. The BMI heritability increased from 75% to 78.8%.ConclusionThe results confirm the hypothesis that the additive genetic variance of BMI has increased strongly during the obesity epidemic. This suggests that the obesogenic environment has enhanced the influence of adiposity related genes.

BackgroundAfter the worldwide steep increase in child and adolescent overweight and obesity during the last decades, there is now evidence of a levelling off in the prevalence in many countries in the Western world.AimTo examine whether there still is a plateau in the prevalence of overweight and obesity in Danish children and adolescents, or whether the prevalence is decreasing or rising again.MethodsThe trends in the prevalence rates were based on three data sets providing comparable repeated estimates: 1) the Danish Health Visitors Child Health Database (DHVCHD) with measurements on infant and childhood height and weight from 2002 to 2011 (n up to 39,984), 2) the Danish National Birth Cohort (DNBC) with maternal reports of measured infant and childhood height and weight from 1998 to 2010 (n up to 56,826) and 3) the Danish part of the Health Behaviour in School-aged Children survey (HBSC) with self-reported information on adolescent height and weight from the years 2002 to 2010 (n = 16,557). Overweight and obesity were categorized according to WHO growth standards. Trends were assessed by repeated point estimates and linear regression analyses providing regression coefficients for changes in per cent per year with 95% confidence intervals (CI).ResultsThe prevalence rates of overweight and obesity for infants, children and adolescents showed a mixed pattern of decline, stability and increase (ranging from -1.10 through 0.29 per cent per year with CI’s from -3.10 through 2.37). Overall, there were no consistent statistically significant trends upwards or downwards, although some significant downward trends in childhood and adolescence were observed.ConclusionThis study, based on data from 1998 through 2011, showed that the prevalence rates of overweight and obesity among Danish infants, children and adolescents were largely still on a plateau with tendencies for a decline among children and adolescents.

Background and objectivesThere is no doubt that the dramatic worldwide increase in obesity prevalence is due to changes in environmental factors. However, twin studies suggest that genetic differences are responsible for the major part of the variation in body mass index (BMI) and other measures of body fatness within populations. Several recent studies suggest that the genetic effects on adiposity may be stronger when combined with presumed risk factors for obesity. We tested the hypothesis that a higher prevalence of obesity and overweight and a higher BMI mean is associated with a larger genetic variation in BMI.MethodsThe data consisted of self-reported height and weight from two Danish twin surveys in 1994 and 2002. A total of 15,017 monozygotic and dizygotic twin pairs were divided into subgroups by year of birth (from 1931 through 1982) and sex. The genetic and environmental variance components of BMI were calculated for each subgroup using the classical twin design. Likewise, the prevalence of obesity, prevalence of overweight and the mean of the BMI distribution was calculated for each subgroup and tested as explanatory variables in a random effects meta-regression model with the square root of the additive genetic variance (equal to the standard deviation) as the dependent variable.ResultsThe size of additive genetic variation was positively and significantly associated with obesity prevalence (p = 0.001) and the mean of the BMI distribution (p = 0.015). The association with prevalence of overweight was positive but not statistically significant (p = 0.177).ConclusionThe results suggest that the genetic variation in BMI increases as the prevalence of obesity, prevalence of overweight and the BMI mean increases. The findings suggest that the genes related to body fatness are expressed more aggressively under the influence of an obesity-promoting environment.