Relation of Serial Changes in Childhood Body-Mass Index to Impaired Glucose Tolerance in Young Adulthood

By S. Bhargava, H. Sachdev, C. Fall, C. Osmond, R. Lakshmy, D. Barker, S. D. Biswas, S. Ramji, D. Prabhakaran, K. Reddy. New England Journal of Medicine, 2004

1,050 citations recorded by the source corpus.

BACKGROUND The risk of type 2 diabetes mellitus is increased in people who have low birth weights and who subsequently become obese as adults. Whether their obesity originates in childhood and, if so, at what age are unknown. Understanding the origin of obesity may be especially important in developing countries, where type 2 diabetes is rapidly increasing yet public health messages still focus on reducing childhood “undernutrition.” METHODS We evaluated glucose tolerance and plasma insulin concentrations in 1492 men and women 26 to 32 years of age who had been measured at birth and at intervals of three to six months throughout infancy, childhood, and adolescence in a prospective, population-based study. RESULTS The prevalence of impaired glucose tolerance was 10.8 percent, and that of diabetes was 4.4 percent. Subjects with impaired glucose tolerance or diabetes typically had a low body-mass index up to the age of two years, followed by an early adiposity rebound (the age after infancy when body mass starts to rise) and an accelerated increase in body-mass index until adulthood. However, despite an increase in body-mass index between the ages of 2 and 12 years, none of these subjects were obese at the age of 12 years. The odds ratio for disease associated with an increase in the body-mass index of 1 SD from 2 to 12 years of age was 1.36 (95 percent confidence interval, 1.18 to 1.57; P<0.001). CONCLUSIONS There is an association between thinness in infancy and the presence of impaired glucose tolerance or diabetes in young adulthood. Crossing into higher categories of body-mass index after the age of two years is also associated with these disorders.

Subfields: Endocrinology, Diabetes and Metabolism, Pediatrics, Perinatology and Child Health, Public Health, Environmental and Occupational Health

View Paper: https://www.semanticscholar.org/paper/7dbb10fe5e2603e10dd67488fd1ff2dd9070b7cb

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Citations in the corpus

The Developmental Origins of Adult Disease (2004, result): “This new observation has now been replicated in a longitudinal study in Delhi, India [40].”
Worldwide trends in diabetes prevalence and treatment from 1990 to 2022: a pooled analysis of 1108 population-representative studies with 141 million participants (2024, neutral): “56,57 Given the disabling and fatal consequences of diabetes, preventing its onset and delaying its complications through improving diet and treatment are essential for better population health throughout the world.”
The developmental origins of chronic adult disease (2004, background): “This new observation has now been replicated in a longitudinal study in Delhi, India (40).”
Early life events and their consequences for later disease: A life history and evolutionary perspective (2007, background): “Other studies have suggested that, rather that rapid infant growth being the most significant factor, it is prolonged impaired infant growth followed by rapid growth in childhood (Bhargava et al., 2004; Eriksson et al., 2003).”
Cardiovascular Diseases in India: Current Epidemiology and Future Directions (2016, neutral): “In the New Delhi Birth Cohort study, rebound adiposity and weight gain during childhood between the ages of 2 and 12 have been shown to be related to a higher propensity to develop dysglycemia as young adults.(84) Data generated from the ongoing intergenerational cohort study involving children and ”
Fetal Origins of Adult Disease (2011, neutral): “Since Barker’s original observations, umerous epidemiologic and human studies, further einforced by animal models, have provided a plethora of upport.(12,19,24-31) Mice, rats, sheep, and monkeys have een subjected to adverse conditions during gestation to imic the human condition.”