Determining Origins and Causes of Childhood Obesity via Mendelian Randomization Analysis 英文参考文献.docVIP
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Determining Origins and Causes of Childhood Obesity via Mendelian Randomization Analysis 英文参考文献
Perspectives
Determining Origins and Causes of
Childhood Obesity via Mendelian
Randomization Analysis
Eric L. Ding, Frank B. Hu
*
C
hildhood obesity has become a
serious public health problem
worldwide. The United States
Linked Research Article
ages nine to 11 was stronger among
mother–offspring pairs than among
father–offspring pairs. This ?nding
suggests that the maternal in?uence
on offspring adiposity extends beyond
genetic contributions alone—providing
some support to the developmental
overnutrition hypothesis. However,
such evidence for this hypothesis is
indirect, as the ?ndings could be
explained by the in?uence of other
maternally predominant factors such as
breast-feeding. Therefore, Lawlor and
colleagues undertook a second, more
sophisticated analysis using a previously
established gene of adult and
This Perspective discusses the
following new study published inPLoS
Medicine:
Lawlor DA, Timpson NJ, Harbord RM,
Leary S, Ness A, et al. (2008) Exploring the
developmental overnutrition hypothesis
using parental–offspring associations
andFTO as an instrumental variable.
PLoS Med 5(3): e33. doi:10.1371/journal.
pmed.0050033
Using parental–offspring associations
and theFTO gene as an instrumental
variable for maternal adiposity, Debbie
Lawlor and colleagues found that
greater maternal BMI during offspring
development does not appear to have
a marked effect on offspring fat mass at
age 9–11.
Centers for Disease Control and
Prevention estimates that one in three
children and adolescents are currently
overweight/obese [1]. The adverse
complications of childhood obesity
on physical health and psychosocial
development are tremendous [2].
Moreover, pediatric obesity may
substantially increase future burden
of cardiovascular disease and other
morbidities in adulthood [3,4].
Developmental Overnutrition
Hypothesis
childhood obesity, the FTO gene [6], as
an “instrument” of maternal obesity (a
marker for the in utero environment)
via a Mendelian randomization (MR)
anal
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