THE AETIOLOGY OF OBESITY IN CHILDREN <i>A Study of 101 Twin Pairs</i>

Börjeson, Mats

doi:10.1111/j.1651-2227.1976.tb04887.x

Cited by 138 publications

(55 citation statements)

References 13 publications

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“…The Hereditary Abilities Study initiated in 1952 was a comprehensive study performed in the United States to investigate heritability of physical traits, including measures of adiposity (birth weight, body weight, and waist circumference) among monozygous and dizygous twins, which demonstrated that the greater part of variance for these traits was genetically determined (Clark 1956). These findings were consistent with other studies reported over 20 years later indicating a high heritability of body weight among monozygous and dizygous twins (Brook et al 1975;Borjeson 1976;Feinleib et al 1977). However, it became apparent that genetic susceptibility interacts with undefined environmental factors to increase adiposity and body weight, in what has formally become known as a ''gene-environment interaction'' and defined as Fig.…”

Section: Heritability Of Body Weight and Interaction With Environmentsupporting

confidence: 91%

“…This population at one time had a subsistence lifestyle but is now predisposed to weight gain and diabetes as a result of a modern obesogenic lifestyle (Knowler et al 1983(Knowler et al , 1991. Moreover, a number of well-designed studies using both monozygotic and dizygotic twins have provided strong evidence demonstrating that children with obesity susceptibility genes living in an obesogenic environment (adopted family) are at increased risk of developing childhood obesity (Borjeson 1976;Silventoinen and Kaprio 2009;Silventoinen et al 2010). These results are consistent with recent anthropological studies verifying that geneenvironment interactions are responsible for marked differences among populations genetically susceptible to weight gain (Casazza et al 2011).…”

Section: Thrifty Gene Hypothesismentioning

confidence: 99%

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The genetics of childhood obesity and interaction with dietary macronutrients

et al. 2013

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The genes contributing to childhood obesity are categorized into three different types based on distinct genetic and phenotypic characteristics. These types of childhood obesity are represented by rare monogenic forms of syndromic or non-syndromic childhood obesity, and common polygenic childhood obesity. In some cases, genetic susceptibility to these forms of childhood obesity may result from different variations of the same gene. Although the prevalence for rare monogenic forms of childhood obesity has not increased in recent times, the prevalence of common childhood obesity has increased in the United States and developing countries throughout the world during the past few decades. A number of recent genome-wide association studies and mouse model studies have established the identification of susceptibility genes contributing to common childhood obesity. Accumulating evidence suggests that this type of childhood obesity represents a complex metabolic disease resulting from an interaction with environmental factors, including dietary macronutrients. The objective of this article is to provide a review on the origins, mechanisms, and health consequences of obesity susceptibility genes and interaction with dietary macronutrients that predispose to childhood obesity. It is proposed that increased knowledge of these obesity susceptibility genes and interaction with dietary macronutrients will provide valuable insight for individual, family, and community preventative lifestyle intervention, and eventually targeted nutritional and medicinal therapies.

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Section: Heritability Of Body Weight and Interaction With Environmentsupporting

confidence: 91%

Section: Thrifty Gene Hypothesismentioning

confidence: 99%

The genetics of childhood obesity and interaction with dietary macronutrients

et al. 2013

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“…The only other study of overweight twins analysed individual differences among overweight twins rather than analysing the difference between the overweight group and the population. 5 This is a problem because the question is not why one obese person differs slightly in weight from another obese person but rather why obese persons as a group are so much heavier than the rest of the population.…”

Section: Introductionmentioning

confidence: 99%

A genetic analysis of weight and overweight in 4-year-old twin pairs

2001

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OBJECTIVE: Although many twin and adoption studies document genetic in¯uence on individual differences in weight, much less is known about genetic in¯uences on overweight, about the genetic links between weight and overweight, or about the origins of weight and overweight in childhood, an age that might provide a good target for prevention of obesity. We tested the hypothesis that, in early childhood, overweight is as heritable as weight and that weight and overweight are linked genetically. DESIGN: Model-®tting analyses were used to compare monozygotic (MZ) and dizygotic (DZ) twins (same-sex and oppositesex) for weight and overweight. SUBJECTS: The sample included 3636 4-y-old twins born in the UK in 1994. MEASUREMENTS: Heights and weights reported by parents were used to assess weight corrected for height, which yields results similar to body mass index (BMI) but corrects more completely for genetic effects on height. RESULTS: At 4 y of age, genetic factors contributed substantially both to individual differences in weight throughout the distribution and to the mean weight difference between overweight children and the rest of the population. Unlike results later in life, weight and overweight in 4-y-olds also suggest substantial shared family environmental in¯uence. Results are similar for boys and girls. CONCLUSIONS: Overweight is the quantitative extreme of genetic and environmental factors responsible for normal variation in weight in childhood. Genes associated with overweight are likely to be associated with variation in weight throughout the distribution, as assumed by quantitative trait locus (QTL) theory. These ®ndings linking weight and overweight in childhood have far-reaching implications for molecular genetic attempts to identify speci®c genes responsible for genetic in¯uence, for investigating pathways between genes and behaviour, and for intervention and prevention.

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“…Also, studies of the heritability of skinfold thicknesses in children yield similar results. 13,18,19 Adoption studies, on the other hand, show only moderate effects of genes (30 ± 40%) on variation of BMI and skinfolds, and family studies generally yield estimates of heritability intermediate between the twin and adoption studies. 20 Results from longitudinal studies support the suggestions from cross-sectional data that there are effects of genes on BMI that are age-speci®c.…”

Section: Introductionmentioning

confidence: 99%

“…3 ± 12 Heritability seems to be higher at younger ages, at least in cross-sectional studies. 4,7,8 The few studies performed in childhood, 1,13 adolescence, 1,14,15 and young adulthood, 16,17 show heritabilities from 70% to over 90% for BMI. Also, studies of the heritability of skinfold thicknesses in children yield similar results.…”

Section: Introductionmentioning

confidence: 99%

Distribution and heritability of BMI in Finnish adolescents aged 16 y and 17 y: A study of 4884 twins and 2509 singletons

Pietiläinen

Kaprio

Rissanen³

et al. 1999

Int J Obes

143

103

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OBJECTIVE: 1) To estimate the heritability of body mass index (BMI) in twins aged 16 y and 17 y, with a special emphasis on gender-speci®c genetic effects and 2) to compare heights, weights, BMIs, and prevalences of`overweight' (BMI ! ! 25 kgam 2 ) in these twins and in singletons aged 16.5 y. DESIGN: Cross-sectional and longitudinal epidemiological questionnaire study of twins at ages 16 y and 17 y, and cross-sectional study of singletons at age 16.5 y. MEASUREMENTS: BMI (kgam 2 ) was calculated from self-reported heights (m) and weights (kg). SUBJECTS: 4884 twins (2299 boys, 2585 girls) at baseline (age 16 y), 4401 twins (2002 boys, 2399 girls) at age 17 y, and 2509 singletons (1147 boys, 1362 girls) at age 16.5 y. Both twin and singleton samples are nationally representative. RESULTS: At the ages of 16 y and 17 y, genetic effects accounted for over 80% of the interindividual variation of BMI. The correlations for male ± female pairs were smaller than for either male-male or female ± female dizygotic pairs. The singletons, especially the boys, had a higher BMI than the twins. Nine percent of singleton boys, but only 4 ± 6% of twin boys and twin and singleton girls were`overweight' (BMI ! ! 25 kgam 2 ). CONCLUSIONS: Among adolescents, genetic factors play a signi®cant role in the causes of variation in BMI. The genetic modelling suggested that the sets of genes explaining the variation of BMI may differ in males and females. At this age, the twin boys, but not girls, seem to be leaner than singletons. Further follow-up will indicate whether these small differences disappear, and if not, what implications it might have to the generalizability of twin studies.

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THE AETIOLOGY OF OBESITY IN CHILDREN A Study of 101 Twin Pairs

Cited by 138 publications

References 13 publications

The genetics of childhood obesity and interaction with dietary macronutrients

The genetics of childhood obesity and interaction with dietary macronutrients

A genetic analysis of weight and overweight in 4-year-old twin pairs

Distribution and heritability of BMI in Finnish adolescents aged 16 y and 17 y: A study of 4884 twins and 2509 singletons

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