Childhood obesity: time to shrink a parent

Lean, Mike

doi:10.1038/ijo.2009.200

Cited by 17 publications

(6 citation statements)

References 21 publications

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“…It seems possible, as we have suggested previously, 11 that the (inappropriate) dietary habits of today's obese parents, and particularly the mother, are revisited on their children from a young age. 22 A second contribution to the rising prevalence of obesity among today's children, this time unrelated to parental weight and not connected to skew, appears to be a widening variance from early puberty. Variance implies a more general environmental exposure, and involves a broader group of children.…”

Section: Discussion and Limitationmentioning

confidence: 99%

Childhood obesity: evidence for distinct early and late environmental determinants a 12-year longitudinal cohort study (EarlyBird 62)

Mostazir¹,

Jeffery²,

Voss³

et al. 2015

Int J Obes

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Section: Discussion and Limitationmentioning

confidence: 99%

Childhood obesity: evidence for distinct early and late environmental determinants a 12-year longitudinal cohort study (EarlyBird 62)

Mostazir¹,

Jeffery²,

Voss³

et al. 2015

Int J Obes

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“… 40 In line with studies among children, 39 the present study has shown that intergenerational relationships of BMI were strongest between mothers and daughters and between fathers and sons, which may point to epigenetic effects. 41 Conventional genetics does not appear to provide full explanations for obesity. The most powerful common single-gene influences on human obesity, for example, FTO , have only small effects on BMI, increasing risk of obesity by 1.2-fold.…”

Section: Discussionmentioning

confidence: 99%

Contributions of maternal and paternal adiposity and smoking to adult offspring adiposity and cardiovascular risk: the Midspan Family Study

et al. 2015

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ObjectiveObesity has some genetic basis but requires interaction with environmental factors for phenotypic expression. We examined contributions of gender-specific parental adiposity and smoking to adiposity and related cardiovascular risk in adult offspring.DesignCross-sectional general population survey.SettingScotland.Participants1456 of the 1477 first generation families in the Midspan Family Study: 2912 parents (aged 45–64 years surveyed between 1972 and 1976) who had 1025 sons and 1283 daughters, aged 30–59 years surveyed in 1996.Main measuresOffspring body mass index (BMI), waist circumference (WC), cardiometabolic risk (lipids, blood pressure and glucose) and cardiovascular disease as outcome measures, and parental BMI and smoking as determinants. All analyses adjusted for age, socioeconomic status and family clustering and offspring birth weight.ResultsRegression coefficients for BMI associations between father–son (0.30) and mother–daughter (0.33) were greater than father–daughter (0.23) or mother–son (0.22). Regression coefficient for the non-genetic, shared-environment or assortative-mating relationship between BMIs of fathers and mothers was 0.19. Heritability estimates for BMI were greatest among women with mothers who had BMI either <25 or ≥30 kg/m2. Compared with offspring without obese parents, offspring with two obese parents had adjusted OR of 10.25 (95% CI 6.56 to 13.93) for having WC ≥102 cm for men, ≥88 cm women, 2.46 (95% CI 1.33 to 4.57) for metabolic syndrome and 3.03 (95% CI 1.55 to 5.91) for angina and/or myocardial infarct (p<0.001). Neither parental adiposity nor smoking history determined adjusted offspring individual cardiometabolic risk factors, diabetes or stroke. Maternal, but not paternal, smoking had significant effects on WC in sons (OR=1.50; 95% CI 1.13 to 2.01) and daughters (OR=1.42; 95% CI 1.10 to 1.84) and metabolic syndrome OR=1.68; 95% CI 1.17 to 2.40) in sons.ConclusionsThere are modest genetic/epigenetic influences on the environmental factors behind adverse adiposity. Maternal smoking appears a specific hazard on obesity and metabolic syndrome. A possible epigenetic mechanism linking maternal smoking to obesity and metabolic syndrome in offspring is proposed. Individuals with family histories of obesity should be targeted from an early age to prevent obesity and complications.

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“…In summary, the rise in fatness of recent years implies new causes – by implication, factors present now that were not present a generation ago. A recent editorial suggested that the successful prevention of childhood obesity might first mean the management of parental obesity , whether the mechanism lies with epigenetic change prior to birth or with dietary errors afterwards. Whichever, the present data offer novel insights into the relationships between parental and offspring fatness that are not revealed by BMI alone, and which may help explain the metabolic outcomes.…”

Section: Discussionmentioning

confidence: 99%

Gender‐assortative waist circumference in mother–daughter and father–son pairs, and its implications. An 11‐year longitudinal study in children (EarlyBird 59)

et al. 2013

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Childhood obesity: time to shrink a parent

Cited by 17 publications

References 21 publications

Childhood obesity: evidence for distinct early and late environmental determinants a 12-year longitudinal cohort study (EarlyBird 62)

Childhood obesity: evidence for distinct early and late environmental determinants a 12-year longitudinal cohort study (EarlyBird 62)

Contributions of maternal and paternal adiposity and smoking to adult offspring adiposity and cardiovascular risk: the Midspan Family Study

Gender‐assortative waist circumference in mother–daughter and father–son pairs, and its implications. An 11‐year longitudinal study in children (EarlyBird 59)

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