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1.

Background and objectives

There 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.

Methods

The 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.

Results

The 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).

Conclusion

The 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.  相似文献   

2.
Studies have documented substantial increases in obesity throughout most of the industrialized world in recent decades. The majority of explanations for these increases have centred around environmental factors such as the increasing availability of high-fat, high-carbohydrate foods and sedentary lifestyles. This study sought to determine if genetic factors might be contributing to the increases in the proportions of North Americans who are obese and overweight. The body mass index (BMI) for a large sample of two generations of United States and Canadian subjects was correlated with family fertility indicators. Small but highly significant positive correlations were found between the BMIs of family members and their reproduction rates, especially in the case of women. For instance, mothers in the sample (most of whom were born in the 1940s and 50s) who were in the normal or below normal range had an average of 4.3 siblings and 3.2 children, compared with 4.8 siblings and 3.5 children for mothers who were overweight or obese. When combined with evidence from twin and adoption studies indicating that genes make substantial contributions to obesity, this study suggests that recent increases in obesity are partially the result of overweight and obese women having more children than is true for average and underweight women. It is speculated that improvements in medical treatments for conditions associated with obesity--particularly diabetes and heart disease--are making it possible for overweight women to live longer and to be more fertile than was true historically.  相似文献   

3.
Genetic aspects of susceptibility to obesity and related dyslipidemias   总被引:4,自引:0,他引:4  
Obesity has a multifactorial origin. However, although environmental variables undoubtedly play a role in the development of obesity, it is now clear that genetic variation is also involved in the determination of an individual's susceptibility to body fat accumulation. In addition, it is also widely accepted that obesity is not a single homogeneous phenotype. It is also heterogeneous regarding its causes and metabolic complications. The regional distribution of body fat appears to be an important correlate of the metabolic complications that have been related to obesity. Due to their higher accumulation of abdominal fat, men are generally more at risk for the metabolic complications of obesity than women whereas some obese women, with large gluteal-femoral adipose depots may have a cosmetic problem which may not necessarily require medical intervention. Several studies have been conducted to understand the mechanisms by which abdominal obesity is related to diabetes, hypertension and cardiovascular disease. It appears that the increased risk of abdominal obesity is the result of complex hormonal and metabolic interactions. Studies in genetic epidemiology have shown that both total body fatness and the regional distribution of body fat have a significant genetic component. Standardized intervention studies using an identical twin design have shown that individuals that have the same genetic background tend to show similar changes in body fat and in plasma lipoprotein levels when exposed to standardized caloric excess or energy restriction. Finally, although abdominal obesity is a significant risk factor for cardiovascular disease, not every abdominal obese subject will experience metabolic complications, suggesting that some obese individuals may be more susceptible than others. Variation in several genes relevant to lipid and lipoprotein metabolism may alter the relation of abdominal obesity to dyslipoproteinemias. Abdominal obesity should therefore be considered as a factor that exacerbates an individual's susceptibility to cardiovascular disease.  相似文献   

4.
Body mass index (BMI), a simple anthropometric measure, is the most frequently used measure of adiposity and has been instrumental in documenting the worldwide increase in the prevalence of obesity witnessed during the last decades. Although this increase in overweight and obesity is thought to be mainly due to environmental changes, i.e., sedentary lifestyles and high caloric diets, consistent evidence from twin studies demonstrates high heritability and the importance of genetic differences for normal variation in BMI. We analysed self-reported data on BMI from approximately 37,000 complete twin pairs (including opposite sex pairs) aged 20-29 and 30-39 from eight different twin registries participating in the GenomEUtwin project. Quantitative genetic analyses were conducted and sex differences were explored. Variation in BMI was greater for women than for men, and in both sexes was primarily explained by additive genetic variance in all countries. Sex differences in the variance components were consistently significant. Results from analyses of opposite sex pairs also showed evidence of sex-specific genetic effects suggesting there may be some differences between men and women in the genetic factors that influence variation in BMI. These results encourage the continued search for genes of importance to the body composition and the development of obesity. Furthermore, they suggest that strategies to identify predisposing genes may benefit from taking into account potential sex specific effects.  相似文献   

5.
Recurrent genomic imbalances at 16p11.2 are genetic risk factors of variable penetrance for developmental delay and autism.Recently,16p11.2 (chr16:29.5 Mb-30.1 Mb) deletion has also been detected in individuals with early-onset severe obesity.The penetrance of 16p11.2deletion as a genetic risk factor for obesity is unknown.We evaluated the growth and body mass characteristics of 28 individuals with 16p11.2(chr16:29.5 Mb-30.1 Mb) deletion originally ascertained for their developmental disorders by reviewing their medical records.We found that nine individuals could be classilied as obese and six as overweight.These individuals generally had early feeding and growth difficulties,and started to gain excessive weight around 5-6 years of age.Thirteen out of the 18 deletion carriers aged 5 years and older (72%) were overweight or obese,whereas only two of 10 deletion carriers (20%) younger than five were overweight or obese.Males exhibited more severe obesity than females.Thus,the obesity phenotype of 16p11.2 deletion carriers is of juvenile onset,exhibited an age.and gender-dependent penetrance.16p11.2 deletion appears to predispose individuals to juvenile onset obesity and in this case are similar to the well-described Prader-Willi syndrome (PWS).Early detection of this deletion will provide opportunity to prevent obesity.  相似文献   

6.
The aim of the current study was to investigate the importance of genetic and environmental effects in the variation of body mass index, and to investigate linkage for obesity to previously reported candidate regions on chromosome 2 and 10. A sample of 1422 twin pairs from the population based Swedish Twin Registry was used in order to estimate the genetic and environmental effects in the variation of body mass index by means of structural equation modeling. A selection of those, 51 concordant and 155 discordant for obesity, was used for the linkage analysis by implementing the "combined" Haseman-Elston approach. Heritability of body mass index ranged from 59-70%, implying that genetic effects were of importance for the variation of obesity, and there were significant sex and age differences. Linkage could not be verified in candidate regions of chromosomes 2 and 10, indicating that these genetic variants have a significant effect in extreme obese populations rather than in moderately obese Caucasians. However, the results were sensitive to issues related to power, minor effects of the genes, ethnic differences and the complex mechanism underlying obesity.  相似文献   

7.
Objective: To understand the overlap between the etiology of obesity and normal variation in BMI in children. Methods and Procedures: Height and weight data were available from a large UK representative sample of twins: 2,342 same‐sex pairs at 7 years and 3,526 same‐sex pairs at 10 years. The twin method and model‐fitting techniques were used to estimate genetic and environmental contributions to BMI. DeFries‐Fulker (DF) extremes analysis was used to investigate genetic and environmental influences on the mean difference between obese and normal‐weight children. Obesity was classified using the International Obesity Task Force (IOTF) criteria. Results: At both ages, BMI and obesity were highly heritable (0.60–0.74) and only modestly influenced by shared environmental factors (0.12–0.22). Extremes analyses indicated that genetic and environmental influences on obesity are quantitatively and qualitatively similar to those operating across the range of BMI. Discussion: Obesity is the extreme of the same genetic and environmental factors responsible for variation throughout the distribution of BMI. This finding implies that genes that influence obesity will also be associated with BMI in the normal range, and similar environmental influences will affect BMI in the clinical and normal range. Knowing that obesity is influenced by the same genetic and environmental factors that affect weight at all levels has implications for investigating the mechanisms for weight gain and developing interventions for weight control.  相似文献   

8.
Recent studies have shown major gene effects for obesity in randomly ascertained families. To investigate the familial aggregation of a specific subset of obesity, which is particularly prone to medical complications, families with morbid obesity were studied. This condition occurs in 1%-2%of the population and is defined as 45.5 kg (100 pounds) or more over ideal weight. First-degree relatives of 221 morbidly obese probands (1560 adults) were identified, and height and weight (current and greatest) were obtained from each family member. Morbid obesity occurred in the family members of the probands 8 times more often than in the general population. Of the morbidly obese probands, 48% had one or more first-degree relatives who were also morbidly obese compared to a 6% population estimate. By the ages of 20–24, 12% of the morbidly obese probands were already 45.5 kg or more overweight, and 45% were 22.7 kg (50 pounds) or more overweight. There was little difference in the prevalence of familial morbid obesity by the gender of the probands: 47% of the male probands and 48% of the female probands had another morbidly obese relative, while 67% and 53% of the early onset (before age 25) male and female probands, respectively, had one or more first-degree relatives who were also morbidly obese. In addition to the extreme degree of familial aggregation, the prevalence of morbid obesity in parent-offspring sets was calculated within the morbidly obese families. Morbidly obese families who have one or two morbidly obese parents have a 2.6 times increased risk (p<0.002) of having one or more morbidly obese adult offspring, compared to families who have neither parent morbidly obese. Evidence for trimodality of the body mass index distribution was found for each gender (p = 0.0006 for male relatives and p = 0.075 for female relatives). The strong familial aggregation of morbid obesity indicates the need for further understanding of the genetic determinants of this extreme clinical disorder and how environmental factors affect the genetic expression of the trait. (OBESITY RESEARCH 1993;1:261–270)  相似文献   

9.
Twin studies have been adopted for decades to disentangle the relative genetic and environmental contributions for a wide range of traits. However, heritability estimation based on the classical twin models does not take into account dynamic behavior of the variance components over age. Varying variance of the genetic component over age can imply the existence of gene–environment (G × E) interactions that general genome-wide association studies (GWAS) fail to capture, which may lead to the inconsistency of heritability estimates between twin design and GWAS. Existing parametric G × E interaction models for twin studies are limited by assuming a linear or quadratic form of the variance curves with respect to a moderator that can, however, be overly restricted in reality. Here we propose spline-based approaches to explore the variance curves of the genetic and environmental components. We choose the additive genetic, common, and unique environmental variance components (ACE) model as the starting point. We treat the component variances as variance functions with respect to age modeled by B-splines or P-splines. We develop an empirical Bayes method to estimate the variance curves together with their confidence bands and provide an R package for public use. Our simulations demonstrate that the proposed methods accurately capture dynamic behavior of the component variances in terms of mean square errors with a data set of >10,000 twin pairs. Using the proposed methods as an alternative and major extension to the classical twin models, our analyses with a large-scale Finnish twin data set (19,510 MZ twins and 27,312 DZ same-sex twins) discover that the variances of the A, C, and E components for body mass index (BMI) change substantially across life span in different patterns and the heritability of BMI drops to ∼50% after middle age. The results further indicate that the decline of heritability is due to increasing unique environmental variance, which provides more insights into age-specific heritability of BMI and evidence of G × E interactions. These findings highlight the fundamental importance and implication of the proposed models in facilitating twin studies to investigate the heritability specific to age and other modifying factors.  相似文献   

10.
Individuals with "metabolically benign" obesity (obesity unaccompanied by hypertension, dyslipidemia, and diabetes) are not at elevated 10-year risk of cardiovascular disease (CVD) compared to normal weight individuals. It remains unclear whether these obese individuals or normal weight individuals with clustering of cardiometabolic factors display heightened immune activity. Therefore, we characterized levels of acute-phase reactants (C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), white blood cell (WBC) count), adhesion molecules (E-selectin, vascular cell adhesion molecule-1), and coagulation products (fibrinogen, plasminogen activator inhibitor-1 (PAI-1)) among four body size phenotypes (normal weight with 0/1 vs. ≥2 metabolic syndrome components/diabetes and overweight/obesity with 0/1 vs. ≥2 metabolic syndrome components/diabetes) in cross-sectional analyses of 1,889 postmenopausal women from the Women's Health Initiative Observational Study (WHI-OS) nested case-control stroke study. Higher levels of all three inflammatory marker categories were found among women with overweight/obesity or ≥2 metabolic syndrome components or diabetes. Compared to normal weight women with 0 or 1 metabolic syndrome components, normal weight women with ≥2 metabolic syndrome components or diabetes were more likely to have ≥3 inflammatory markers in the top quartile (multivariate odds ratio (OR) 2.0, 95% confidence interval (CI): 1.3-3.0), as were overweight/obese women with 0 or 1 metabolic syndrome components (OR 2.3; 95% CI: 1.5-3.5). Overweight/obese women with ≥2 metabolic syndrome components or diabetes had the highest OR (OR 4.2; 95% CI: 2.9-5.9). Despite findings that metabolically benign obese individuals are not at increased 10-year risk of CVD compared to normal weight individuals, the current results suggest that overweight/obese women without clustering of cardiometabolic risk factors still possess abnormal levels of inflammatory markers.  相似文献   

11.
Data about metabolic syndrome (MetS) in children is limited in China. We aimed to assess the prevalence of MetS related components, and their association with obesity. Data were collected as part of a representative study on MetS among 19593 children, aged 6–18 years old in Beijing. General obesity was assessed by body mass index (BMI) and central obesity by waist circumference. Finger capillary blood tests were used to assess triglyceride (TG), total cholesterol (TC) and impaired fasting glucose (IFG). Vein blood samples were collected from a subsample of 3814 children aged 10–18 years to classify MetS. MetS was defined according to the International Diabetes Federation 2007 definition. The associations between MetS related components and the degree and type of obesity were tested using logistic regression models. The prevalence of overweight, obesity, high blood pressure, elevated TG, TC and IFG were13.6%, 5.8%, 8.5%, 8.8%, 1.2% and 2.5%, respectively. Compared with normal weight children, overweight and obese children were more likely to have other MetS related components. In the subsample of 3814 children aged 10–18 years, the prevalence of MetS was much higher in obese subjects than in their normal weight counterparts (27.6% vs. 0.2%). Children with both general and central obesity had the highest prevalence of MetS. Compared with normal weight children, overweight and obese children were more likely to have MetS (overweight: OR = 67.33, 95%CI = 21.32–212.61; obesity: OR = 249.99, 95% CI = 79.51–785.98). Prevalence of MetS related components has reached high level among Beijing children who were overweight or obese. The association between metabolic disorders and obesity was strong.  相似文献   

12.
Variance components models for gene-environment interaction in twin analysis.   总被引:10,自引:0,他引:10  
Gene-environment interaction is likely to be a common and important source of variation for complex behavioral traits. Often conceptualized as the genetic control of sensitivity to the environment, it can be incorporated in variance components twin analyses by partitioning genetic effects into a mean part, which is independent of the environment, and a part that is a linear function of the environment. The model allows for one or more environmental moderator variables (that possibly interact with each other) that may i). be continuous or binary ii). differ between twins within a pair iii). interact with residual environmental as well as genetic effects iv) have nonlinear moderating properties v). show scalar (different magnitudes) or qualitative (different genes) interactions vi). be correlated with genetic effects acting upon the trait, to allow for a test of gene-environment interaction in the presence of gene-environment correlation. Aspects and applications of a class of models are explored by simulation, in the context of both individual differences twin analysis and, in a companion paper (Purcell & Sham, 2002) sibpair quantitative trait locus linkage analysis. As well as elucidating environmental pathways, consideration of gene-environment interaction in quantitative and molecular studies will potentially direct and enhance gene-mapping efforts.  相似文献   

13.
Globally 30% of adults are overweight or obese. The white adipocyte is a major component of adipose tissue, and as the obesity epidemic increases it is critically important to understand the factors determining adipocyte development and function. Adipogenesis has two distinct phases; determination of the adipocyte from a multipotent stem cell, and terminal differentiation of a pre-adipocyte into a mature adipocyte. The environment encountered in early life can alter adipocyte number and size and potentially impact upon adipocyte endocrine function in adulthood. These alterations may contribute to the pathophysiology of chronic diseases and thus targeted therapy of the adipocyte has great potential for treating the current obesity epidemic.  相似文献   

14.
Social networks theory suggests obesity is “contagious” within peer groups in that known friends highly influence weight. On the other hand, an alternative model suggests that observable weight distributions affect perception of one's own obesity level. We examine whether the BMI levels of the most obese classmates in the individual student's grade by gender is positively associated with “under‐assessment” of obesity and overweight (i.e., independently measured obesity or overweight, but subjective self‐assessment of normal weight). The data are the 2004–2005 School Physical Activity and Nutrition III (SPAN), a stratified, multistage probability sample of 4th, 8th, and 11th grade public school children in Texas. We used logistic regression to test whether the gender‐specific 85th percentile BMI level within the individual student's grade at their school is positively associated with “under‐assessment” of obesity and overweight. The results show that students are much more likely to under‐assess their own weight if the gender‐specific 85th percentile BMI level is higher in their grade at their school. These data suggest that observable weight distributions play a key role in the obesity epidemic.  相似文献   

15.
A recurring criticism of the twin method for quantifying genetic and environmental components of human differences is the necessity of the so-called "equal environments assumption" (EEA) (i.e., that monozygotic and dizygotic twins experience equally correlated environments). It has been proposed to test the EEA by stratifying twin correlations by indices of the amount of shared environment. However, relevant environments may also be influenced by genetic differences. We present a model for the role of genetic factors in niche selection by twins that may account for variation in indices of the shared twin environment (e.g., contact between members of twin pairs). Simulations reveal that stratification of twin correlations by amount of contact can yield spurious evidence of large shared environmental effects in some strata and even give false indications of genotype x environment interaction. The stratification approach to testing the equal environments assumption may be misleading and the results of such tests may actually be consistent with a simpler theory of the role of genetic factors in niche selection.  相似文献   

16.
The prevalence for excessive weight has also been increasing dramatically in Portugal over the last decades. The consequences for families as well as for the publicly funded Portuguese health care system are a matter of policy interest. This paper uses an econometric model to compute the fraction of the national out-of-pocket health care expenditures attributable to overweight and obesity among Portuguese adults. Given that public health care system pays for a substantial share of the national health care expenditures, the estimated the out-of-pocket expenditures is only a share of the total expenditures. Per-capita expenditures and the burden that obesity and overweight impose on families are also estimated. Two waves of the Portuguese National Health Survey (NHS), namely; 1995/1996 and 1998/1999 are considered. The results suggest that out-of-pocket expenditures due to excess weight have increased sharply during these 3 years. The two-part model estimates suggest that the obese and overweight are more likely to incur out-of-pocket health care expenditures but, in the restricted sample of those that incur expenditures, there is weak or no evidence that the obese or overweight spend, on average, more than those of normal weight. Overall, it is estimated that in 1995/1996, more than 1.8% out-of-pocket health care expenditures were attributable to obesity and 2% to overweight (although not statistically significant). The estimated percentages are over 2.9% for obesity and 4% for overweight in 1998/1999. Combined, the estimated attributable percentage of national out-of-pocket expenditures due to excess weight was 3.8% in 1995/1996 and 6.9% in 1998/1999. Per-capita expenditures due to obesity or overweight are small, on average, in absolute terms, but they can be a significant cost for low income families. With respect to public policy concerns, the results suggest that measures which only slightly increase the out-of-pocket health care expenditures of being obese (overweight) are likely to be inefficient.  相似文献   

17.
Genetic and environmental aspects are recognized in the obesity field and attempts to elucidate multiple genes and gene/environment interactions are necessary. In rare cases of monogenic obesities, genetic tools have proved extremely powerful for identifying the genes responsible and for defining new syndromes. Abnormalities of genes involved in the leptin/melanocortin axis have been described. In common obesity, most studies include the search for genotype/phenotype associations without taking into account the influence of environment (diet, sedentary lifestyle) in the relationship. Many genes and candidate regions have been proposed to be involved in the determinism of human obesity. Among the limitations to this integrated approach, one can cite the difficulty of having large enough samples as well as biocomputing tools that are still in their infancy for accessing the question of multiple interactions with no "a priori hypotheses". This picture will probably change rapidly in the future. The purpose of this paper is to present some examples of the knowledge acquired in the field of obesity genetics and the new ongoing tools and developments that aim at studying the contribution of genes to obesity and their response to environmental changes. The capacity for studying multiple genes at once at the DNA or RNA levels is rapidly growing. Finally, tremendous progress in biocomputing will allow the integration of information from different sources (i.e. environment, phenotype, genotype, gene expression) and thus improve our ability to deal with complexity. Examples of these approaches exist in humans and in animal models.  相似文献   

18.
We develop a model to estimate the influence of child and parental characteristics on the likelihood that a child will become an obese or overweight youth. We use this model to test whether it is possible to forecast obesity and overweight among youth. Comparing Receiver Operating Characteristic (ROC) scores from these forecasts, we find that a model using childhood covariates does as well in forecasting youth obesity and overweight as a model using the covariate values contemporaneous with the youth obesity and overweight outcomes. The datasets used in this paper, the National Longitudinal Survey of Youth (NLSY79) and the NLSY79 Children and Young Adults, provide data from 1986 to 2002, allowing for the study of a child's transition to and from obesity or overweight over a long period. Explanatory variables that significantly influence the likelihood of youth obesity or overweight outcomes include the mother's obesity status and education, the youth's mental health, and certain demographic features including race, sex, and family size. These factors provide potential targets for policies that could be implemented early in life among children most likely to become obese or overweight.  相似文献   

19.
Childhood overweight and obesity is a major public health challenge for policymakers in many countries. As the most common supervisors of children’s activities, parents have a potentially important role to play in obesity prevention. However, a precondition for parents to improve their children’s diets, encourage them to be more physically active, or take them to see a doctor about their weight is for the parent to first recognize that their child is overweight or obese. This paper examines the extent of parental misclassification of child weight status, and its correlates, focusing on the role of parental education and the parent’s own obesity status. We find evidence that, among non-obese parents, those who are better-educated report their child’s weight status more accurately, but among obese parents, the better-educated are 45.18% more likely than parents with lower secondary education to give a false negative report of their child’s overweight/obesity; this may reflect social desirability bias.  相似文献   

20.
The aim of this article was to investigate the prevalence of overweight and obesity using selected anthropometric variables in a sample of hospitalized coronary heart disease (CHD) patients in Croatia (N = 1,298). Prevalence of overweight and obesity in surveyed patient population was high: 48.2% of participants were overweight and 28.6% were obese according to their body mass index; measured through waist-to-hip ratio 54.5% of participants were centrally obese. These data on prevalences of overweight, obesity and central obesity show that although there are some reassuring trends, there is still considerable amount of work to be done if the prevalence of this cardiovascular risk factor is to be reduced further among Croatian CHD patients. While the prevalence of obesity seems to be on the decline, the prevalence of overweight is rising, which may be just an early warning sign of an incoming wave of obesity epidemic in future years.  相似文献   

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