To the Editor.—
Taveras et al(1) report on a prospective cohort of 559 children with
a mean birth weight of 3.55 kg and mean gestational age of 39.8 weeks.
They found that increased weight-for-length z scores at birth were
associated with increased odds of obesity at 3 years of age. This is
consistent with a systematic review of 24 studies concluding infants with
the highest body mass index are at increased risk for subsequent
obesity(2). The implications are clear: increased risk for metabolic
syndrome and cardiovascular disease.
While these findings might be somewhat intuitive and expected, it
doesn’t easily explain why full-term small for gestational age (SGA) or
pre-term infants are also at risk for cardiovascular disease. Since
Barker proposed the “fetal origins hypothesis” of cardiovascular
disease(3,4), much literature has been focused on the developmental
origins of subsequent health. For instance, low birth weight and/or
prematurity is associated in adults with hypertension(5), insulin
resistance(6,7), dyslipidema(8), and higher body mass index(9-11). Is
there then a common factor that presages obesity and/or the components of
the metabolic syndrome in SGA, pre-term, or large full-term infants?
The Taveras study would seem to indicate that in full-term infants,
obesity is heralded by rapid weight gain in infancy, particularly that
which occurs in the first 6 months(1). In addition, the adverse
consequence of accelerated growth on cardiometabolic status in SGA and pre
-term infants may be comparable or perhaps even greater. For instance,
greater weight or linear gain in the first 2 weeks of life was associated
with lower flow-mediated endothelium-dependent dilation, irrespective of
normal or low birth weight(12). Similarly, accelerated post-natal growth
in pre-term infants is associated with increased subcutaneous and total
adiposity relative to control term infants(13).
Singhal and Lucas propose the “growth acceleration” hypothesis to
explain the increased risk of cardiovascular disease associated with rapid
weight gain regardless of birth weight(14). In fact epidemiological data
supports this hypothesis in the form of a “catch-up fat” phenotype that
can be relevant at any age(15).
It thus appears that the characteristic phenotype common to
cardiometabolic risk, regardless of birth size, is rapid weight gain. We
agree that infancy is a crucial period in obesity prevention and may even
be more crucial in low birth weight infants born premature or SGA. Rapid
weight gain should be prevented, and a careful re-evaluation of the risks
and benefits of nutritional therapy should be undertaken in pre-term and
SGA infants.
Y. Sammy Choi, MD, FAAP, FACP;
Departments of Medicine, Pediatrics, and Research;
Womack Army Medical Center,
Fort Bragg, NC 28310
Carl E. Hunt, MD;
Professor of Pediatrics;
Uniformed Services University of the Health Sciences,
Bethesda, MD 20814
The views expressed herein are those of the authors and not to be
construed as representing the official views of the Department of Defense.
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Gillman MW. Weight status in the first 6 months of life and obesity at 3
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big or growing fast: systematic review of size and growth in infancy and
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Conflict of Interest:
None declared