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. 2014 Feb 13;9(2):e86914. doi: 10.1371/journal.pone.0086914

Table 1. Risk factors investigated in the study.

Risk factor Hypotheses
Prepartum
Smoking during pregnancy Own causal effect (risk factor) e.g. through fetal growth retardation and subsequent developmental adaptations [46], [47].
Possible confounder: Parental energy intake [47], parental socioeconomic status [46].
Gestational weight gain Own causal effect (risk factor) e.g. through shared genetic factors (on weight gain), shared environment (e.g. diet), fetal programming [48], [49].
Possible confounder: Maternal BMI [49].
Gestational diabetes Own causal effect (risk factor) e.g. through shared genetic factors, shared environment, fetal programming [50].
Possible confounder: Maternal BMI.
Peripartum
Birth weight Own causal effect (risk factor) reflecting fetal growth, programming for lean mass and fat distribution [32].
Possible artifact due to high correlation of BMI and lean body mass [32].
Caesarian section Own causal effect (risk factor) e.g. through differences in colonizing bacteria species [34].
Possible confounder: Maternal BMI, maternal smoking during pregnancy, breastfeeding [34].
Postpartum
Breastfeeding (initiation and duration) Own causal effect (protective factor) e.g. through nutritional programming [51], [52], moderation of genetic effects [53], reduced risk of overfeeding [54].
Known confounder: parental obesity, maternal smoking during pregnancy, parental socioeconomic status; might completely remove the effect [55].
Association possibly artificial due to lower breastfeeding success in obese and/or smoking mothers [10], [26].
Early introduction of solid foods Own causal effect (risk factor) e.g. through nutritional programming [56].
Possible confounder: Parental socioeconomic status [57], breastfeeding [58], [59].