Large Maternal Weight Loss From Obesity Surgery Prevents Transmission of Obesity to Children Who Were Followed for 2 to 18 Years

Kral, John G.; Biron, Simon; Simard, Serge; Hould, Frédéric‐Simon; Lebel, Stéfane; Marceau, Simon; Marceau, Picard

doi:10.1542/peds.2006-1379

Cited by 337 publications

(203 citation statements)

References 38 publications

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“…83 Maternal weight loss by pre-pregnancy bariatric surgery prevents transmission of obesity to children compared with the offspring of mothers who did not undergo the surgery and remained obese. 84 Gestational weight gain irrespective of pre-pregnancy body mass is positively associated with obesity at 3 years. 85 Higher birth weight is linked by strong epidemiological evidence to childhood, adolescent and adult obesity, as demonstrated by the large cohort studies showing a greater prevalence of overweight in individuals born large 32 as well as more recent clinical studies showing that mothers with a higher pre-pregnant body mass index or a larger mid-upper-arm circumference during pregnancy tend to have children with greater adiposity at the age of 9 years.…”

Section: The 'Early-life Hypernutrition' Pathwaysmentioning

confidence: 97%

Developmental and epigenetic pathways to obesity: an evolutionary-developmental perspective

2008

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Although variation in individual lifestyle and genotype are important factors in explaining individual variation in the risk of developing obesity in an obesogenic environment, there is growing evidence that developmentally plastic processes also contribute. These effects are mediated at least in part through epigenetic processes. These developmental pathways do not directly cause obesity but rather alter the risk of an individual developing obesity later in life. At least two classes of developmental pathway are involved. The mismatch pathway involves the evolved adaptive responses of the developing organism to anticipated future adverse environments, which have maladaptive consequences if the environment is mismatched to that predicted. This pathway can be cued by prenatal undernutrition or stresses that lead the organism to forecast an adverse future environment and change its developmental trajectory accordingly. As a result, individuals develop with central and peripheral changes that increase their sensitivity to an obesogenic environment. It provides a model for how obesity emerges in populations in rapid transition, but also operates in developed countries. There is growing experimental evidence that this pathway can be manipulated by, for example, postnatal leptin exposure. Secondly, maternal diabetes, maternal obesity and infant overfeeding are associated with a greater risk of later obesity. Early life offers a potential point for preventative intervention.

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Section: The 'Early-life Hypernutrition' Pathwaysmentioning

confidence: 97%

Developmental and epigenetic pathways to obesity: an evolutionary-developmental perspective

2008

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“…Gestational weight gain irrespective of pre-pregnancy weight is positively associated with obesity at the age of 3 years (19) and even moderate weight gain between successive pregnancies has been shown to result in a significant increase in large for gestational age births (20) . However, maternal weight loss through bariatic surgery prevents the transmission of obesity to children compared to the offspring of mothers who did not undergo the surgery and remained obese (21) .…”

Section: The Developmental Origins Of Human Cardio-metabolic Diseasementioning

confidence: 99%

Effect of maternal diet on the epigenome: implications for human metabolic disease

Lillycrop

2011

Proc. Nutr. Soc.

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The rapid increase in the incidence of chronic non-communicable diseases over the past two decades cannot be explained solely by genetic and adult lifestyle factors. There is now considerable evidence that the fetal and early postnatal environment also strongly influences the risk of developing such diseases in later life. Human studies have shown that low birth weight is associated with an increased risk of CVD, type II diabetes, obesity and hypertension, although recent studies have shown that over-nutrition in early life can also increase susceptibility to future metabolic disease. These findings have been replicated in a variety of animal models, which have shown that both maternal under-and over-nutrition can induce persistent changes in gene expression and metabolism within the offspring. The mechanism by which the maternal nutritional environment induces such changes is beginning to be understood and involves the altered epigenetic regulation of specific genes. The demonstration of a role for altered epigenetic regulation of genes in the developmental induction of chronic diseases raises the possibility that nutritional or pharmaceutical interventions may be used to modify long-term cardio-metabolic disease risk and combat this rapid rise in chronic non-communicable diseases.Epigenetics: DNA methylation: Fetal development: CVD: ObesityThe incidence of chronic non-communicable disease has risen sharply over the last 20 years with an estimated 18 million people dying from CVD per year (1) . This rise in CVD has been amplified by a rapid rise in the rate of obesity and type II diabetes across the world, which are major risk factors for CVD. This increase in the incidence of chronic non-communicable diseases over the past two decades cannot be explained solely by genetic and adult lifestyle factors. There is now substantial evidence that the fetal and early postnatal environment strongly influences the risk of developing cardio-metabolic disease. Epidemiological studies show that a poor intra-uterine environment induced by maternal diet, placental insufficiency or endocrine factors, such as stress, induces changes in the embryo and fetus, which increase its future risk of a range of non-communicable diseases (2) . These findings have been replicated in animal models where restricted nutrition during pregnancy induces dyslipidaemia, obesity, hypertension, hyperinsulinaemia and hyperleptinaemia in the offspring (3,4) . This association between poor intrauterine growth and increased risk of disease in later life may reflect a mismatch between the future environment 'predicted' by the embryo/fetus, based on signals from the mother during gestation, and the actual environment experienced in later life (5) . The mechanism by which cues about nutrient availability in the postnatal environment are transmitted to the fetus and the process by which different, stable phenotypes are induced are beginning to be understood. A number of recent studies suggest that changes in the epigenetic regulation of genes in the embryo ...

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“…1,2 The evidence is now overwhelming that the risk is increased for large for gestational age (LGA) infants to be born to women who are overweight or obese when they become pregnant, who gain excess weight during pregnancy, who smoke during pregnancy, who develop gestational diabetes or who are older at first pregnancy. [1][2][3][4][5][6][7] Being LGA portends a much higher risk of obesity later in childhood and adulthood, with odds ratios as high as 15 compared with normal weight newborns. 1 Black children born LGA were 2.5-fold more likely to be obese at ages 2-5 than average weight babies, and had a 30% prevalence of obesity.…”

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confidence: 99%

“…The consequences of weight loss in obese women before pregnancy on weights of offspring at birth and through young adulthood are shown by the study of Kral et al 4 These authors identified women who had pregnancies before and after they had undergone bariatric surgery. All of the women were very obese at the time of the first pregnancy and had lost an average of over 15 BMI units by the time of the second pregnancy.…”

mentioning

confidence: 99%

Are we attacking the wrong targets in the fight against obesity?: the importance of intervention in women of childbearing age

et al. 2012

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Large Maternal Weight Loss From Obesity Surgery Prevents Transmission of Obesity to Children Who Were Followed for 2 to 18 Years

Cited by 337 publications

References 38 publications

Developmental and epigenetic pathways to obesity: an evolutionary-developmental perspective

Developmental and epigenetic pathways to obesity: an evolutionary-developmental perspective

Effect of maternal diet on the epigenome: implications for human metabolic disease

Are we attacking the wrong targets in the fight against obesity?: the importance of intervention in women of childbearing age

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