Early growth and type 2 diabetes: evidence from the 1946 British birth cohort

Wadsworth, Mej; Butterworth, Suzanne; Marmot, Michael; Ecob, Russell; Hardy, Rebecca

doi:10.1007/s00125-005-0007-4

Cited by 55 publications

(39 citation statements)

References 25 publications

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“…15,16,31,32 We were unable to investigate the levels of blood glucose and insulin in the current study, but our data indicate that children who exhibit early AR are predisposed to future development of insulin resistance due to higher BMI, TG, AI, ApoB, and blood pressure and lower HDL-C in boys and higher ApoB in girls. The mechanism through which early AR is associated with later adverse lipoprotein profiles is unclear, but we speculate that metabolic programming leading to future insulin resistance may operate during the early increase of BMI.…”

Section: Figurementioning

confidence: 64%

Adiposity Rebound and the Development of Metabolic Syndrome

et al. 2014

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OBJECTIVE: The age of adiposity rebound (AR) is defined as the time at which BMI starts to rise after infancy and is thought to be a marker of later obesity. To determine whether this age is related to future occurrence of metabolic syndrome, we investigated the relationship of the timing of AR with metabolic consequences at 12 years of age. METHODS: A total of 271 children (147 boys and 124 girls) born in 1995 and 1996 were enrolled in the study. Serial measurements of BMI were conducted at the ages of 4 and 8 months and 1, 1.5, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, and 12 years, based on which age of AR was calculated. Plasma lipids and blood pressure were measured at 12 years of age. RESULTS: An earlier AR (<4 years of age) was associated with a higher BMI (≥20) and a lipoprotein phenotype representative of insulin resistance. This phenotype consists of elevated triglycerides, apolipoprotein B, and atherogenic index and decreased high-density lipoprotein cholesterol in boys and elevated apolipoprotein B in girls at 12 years of age. The earlier AR was also related to elevated blood pressure in boys. CONCLUSIONS: This longitudinal population-based study indicates that children who exhibit AR at a younger age are predisposed to future development of metabolic syndrome. Therefore, monitoring of AR may be an effective method for the early identification of children at risk for metabolic syndrome.

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Section: Figurementioning

confidence: 64%

Adiposity Rebound and the Development of Metabolic Syndrome

et al. 2014

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“…This situation is reversed later in childhood, as the BMI rebound (the period after infancy when BMI starts to increase) occurs earlier in persons who later develop type 2 diabetes [5,7]; these individuals have an accelerated increase in BMI thereafter [5,8].…”

Section: Introductionmentioning

confidence: 99%

Childhood BMI trajectories and the risk of developing young adult-onset diabetes

Lammi¹,

Moltchanova²,

Blomstedt³

et al. 2009

Diabetologia

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Aims/hypothesis The aim of this study was to examine the effects of childhood BMI growth dynamics on the risk of developing young adult-onset type 1 and type 2 diabetes. Methods Finnish national healthcare registers were used to identify individuals with diabetes diagnosed between 1992 and 1996 at 15-39 years of age. Non-diabetic control participants were chosen from the National Population Registry. Anthropometric measurements were obtained from the original child welfare clinic records. Only the case-control pairs with sufficient growth data recorded were included in the analyses (218/1,388 for type 1 diabetes [16%] and 64/1,121 for type 2 diabetes [6%]). Two developmental stages in BMI growth (the points of infancy maximum BMI and the BMI rebound) were examined, and conditional logistic regression was applied to the variables of interest.Results The risk for type 1 diabetes increased 1.19-fold per 1 kg/m 2 rise in the infancy maximum BMI (p=0.02). In addition, there was a 1.77-fold increase in the risk for type 2 diabetes per 1 kg/m 2 rise in the level of BMI at the BMI rebound (p=0.04). Higher values of BMI at these points corresponded to a larger BMI gain from birth to that developmental stage. Age at the infancy maximum BMI or age at the BMI rebound did not affect the risk for either type of diabetes. Conclusions/interpretation The BMI gain in infancy among individuals who subsequently developed young adult-onset type 1 diabetes was faster than that of those who remained healthy. The excess BMI gain in individuals who developed young adult-onset type 2 diabetes could already be seen during early childhood.

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“…catch-up growth after onset of early adiposity rebound) seems to confer increased risk for impaired glucose tolerance and type 2 diabetes in adulthood. [28][29][30] Whether children who have an early adiposity rebound had a low-weight gain during infancy because of exposure to a weaning or post-weaning infant diet that is low in fat but high in protein, 31 followed by a childhood diet that is high in fat, is currently controversial. 27 However, as reviewed by Taylor et al, 27 an early age for adiposity rebound has also been recorded in a number of pediatric conditions characterized by high subsequent obesity, including children treated for adrenal 21-hydroxylase deficiency, hypothyroidism, hyperphenylalaninemia and acute lymphoblastic leukemia -all conditions that are generally associated with perturbed growth before the premature adiposity rebound that overlaps with catch-up growth.…”

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confidence: 99%

The thrifty ‘catch-up fat’ phenotype: its impact on insulin sensitivity during growth trajectories to obesity and metabolic syndrome

et al. 2006

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The analyses of large epidemiological databases have suggested that infants and children who show catch-up growth, or adiposity rebound at a younger age, are predisposed to the development of obesity, type 2 diabetes and cardiovascular diseases later in life. The pathophysiological mechanisms by which these growth trajectories confer increased risks for these diseases are obscure, but there is compelling evidence that the dynamic process of catch-up growth per se, which often overlaps with adiposity rebound at a younger age, is characterized by hyperinsulinemia and by a disproportionately higher rate in the recovery of body fat than lean tissue (i.e. preferential 'catch-up fat'). This paper first focuses upon the almost ubiquitous nature of this preferential 'catch-up fat' phenotype across the life cycle as a risk factor for obesity and insulin-related complications -not only in infants and children who experienced catch-up growth after earlier fetal or neonatal growth retardation, or after preterm birth, but also in adults who show weight recovery after substantial weight loss owing to famine, disease-cachexia or periodic dieting. It subsequently reviews the evidence indicating that such preferential catch-up fat is primarily driven by energy conservation (thrifty) mechanisms operating via suppressed thermogenesis, with glucose thus spared from oxidation in skeletal muscle being directed towards de novo lipogenesis and storage in white adipose tissue. A molecular-physiological framework is presented which integrates emerging insights into the mechanisms by which this thrifty 'catch-up fat' phenotype crosslinks with early development of insulin and leptin resistance. In the complex interactions between genetic constitution of the individual, programming earlier in life, and a subsequent lifestyle of energy dense foods and low physical activity, this thrifty 'catch-up fat' phenotype -which probably evolved to increase survival capacity in a hunter-gatherer lifestyle of periodic food shortages -is a central event in growth trajectories to obesity and to diseases that cluster into the insulin resistance (metabolic) syndrome.

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Early growth and type 2 diabetes: evidence from the 1946 British birth cohort

Cited by 55 publications

References 25 publications

Adiposity Rebound and the Development of Metabolic Syndrome

Adiposity Rebound and the Development of Metabolic Syndrome

Childhood BMI trajectories and the risk of developing young adult-onset diabetes

The thrifty ‘catch-up fat’ phenotype: its impact on insulin sensitivity during growth trajectories to obesity and metabolic syndrome

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