The early life nutritional environment and early life stress as potential pathways towards the metabolic syndrome in mid-life? A lifecourse analysis using the 1958 British Birth cohort

C. Delpierre, R. Fantin, C. Barboza-Solis, B. Lepage, M. Darnaudéry, M. Kelly-Irving
BMC Public Health. 2016-08-18; 16(1):
DOI: 10.1186/s12889-016-3484-0

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Delpierre C(1)(2), Fantin R(3)(4), Barboza-Solis C(3)(4)(5), Lepage B(3)(4)(6), Darnaudéry M(7)(8), Kelly-Irving M(3)(4).

Author information:
(1)INSERM, UMR1027, Toulouse, F-31000, France.
(2)Université Toulouse III Paul-Sabatier, UMR1027, Toulouse, F-31000, France.
(3)INSERM, UMR1027, Toulouse, F-31000, France.
(4)Université Toulouse III Paul-Sabatier, UMR1027, Toulouse, F-31000, France.
(5)Universidad de Costa Rica, 2060, San José, Costa Rica.
(6)Department of Epidemiology, Centre Hospitalier Universitaire de Toulouse,Toulouse, France.
(7)Université Bordeaux, Laboratoire NUTRINEURO, UMR 1286, F-33076, Bordeaux,France.
(8)INRA, Lab NUTRINEURO, UMR 1286, F-33076, Bordeaux, France.

BACKGROUND: Lifecourse studies suggest that the metabolic syndrome (MetS) may be
rooted in the early life environment. This study aims to examine the pathways
linking early nutritional and psychosocial exposures and the presence of MetS in
midlife.
METHODS: Data are from the National Child Development Study including individuals
born during 1 week in 1958 in Great Britain and followed-up until now. MetS was
defined based on the National Cholesterol Education Program Adult Treatment Panel
III classification. Mother’s pre-pregnancy body mass index (BMI) was used as a
proxy of the early nutritional environment and Adverse Childhood Experiences
(ACE) as a proxy for early psychosocial stress. Socioeconomic characteristics,
pregnancy and birth conditions were extracted as potential confounders. Adult
health behaviors, BMI, socioeconomic environment and psychological state were
considered as mediating variables. Multivariate models were performed by
including variables sequentially taking a lifecourse approach.
RESULTS: 37.5 % of men and 19.8 % of women had MetS. Participants with an
obese/overweight mother presented a higher risk of MetS than those whose mother
had a normal pre-pregnancy BMI. Men exposed to two ACE or more, and women exposed
to one ACE, were more at risk of MetS compared to unexposed individuals. After
including confounders and mediators, mother’s pre-pregnancy BMI was still
associated with MetS in midlife but the association was weakened after including
participant’s adult BMI. ACE was no longer associated with MetS after including
confounders in models.
CONCLUSIONS: The early nutritional environment, represented by mother’s
pre-pregnancy BMI, was associated with the risk of MetS in midlife. An important
mechanism involves a mother-to-child BMI transmission, independent of birth or
perinatal conditions, socioeconomic characteristics and health behaviors over the
lifecourse. However this mechanism is not sufficient for explaining the influence
of mother’s pre-pregnancy BMI which implies the need to further explore other
mechanisms in particular the role of genetics and early nutritional environment.
ACE is not independently associated with MetS. However, other early life
stressful events such as emergency caesarean deliveries and poor socioeconomic
status during childhood may contribute as determinants of MetS.

 

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