of diet components or patterns associated with higher or lower offspring obesity risk. Nonetheless, some evidence suggests that certain aspects of a mother’s diet quality may influence these outcomes in the next generation.
Dietary components examined to date generally follow those already found to be associated with obesity or related metabolic risks among children and nonpregnant adults. For example, a Project Viva analysis examined associations of maternal sugary beverage intake and child adiposity. Each additional serving per day of sugary drinks (SDs) consumed by mothers during pregnancy was associated with higher child BMI z scores (0.07 units; 95% confidence interval (CI): −0.01 to 0.15), fat mass index (0.15 kg/m2; 95% CI: −0.01 to 0.30), and waist circumference (0.65 cm; 95% CI: 0.01 to 1.28) [58]. Further analyses suggested that the associations were due primarily to maternal, not child, SD intake, and to sugary soda rather than fruit drinks or juice. Interestingly, in the same cohort, maternal intake of non‐nutritive sweeteners during pregnancy also was associated with increased childhood BMI z‐score and body fat from birth to teenage years. This finding aligns with research in other populations suggesting that consumption of artificial sweeteners may promote weight gain rather than preventing it [59].
The traditional Mediterranean diet is characterized by a high intake of olive oil, fruits, vegetables, legumes, nuts, and whole‐grain products; a moderate intake of fish; and only small amounts of red and processed meat. This dietary pattern is low in saturated fat intake and high in monounsaturated fat intake from olive oil; it is rich in fiber, provides a balanced ratio of n‐6/n‐3 essential fatty acids, and contains high amounts of antioxidants. Several epidemiological studies and clinical trials support the role of the Mediterranean diet in preventing obesity, type 2 diabetes mellitus, and metabolic syndrome in adults [60], but the effects of maternal prenatal intake have not been well studied. One analysis examined maternal Mediterranean dietary patterns during pregnancy in two cohorts with different dietary habits and socio‐demographics – the Boston, MA area Project Viva cohort and the Rhea Cohort based in Crete, Greece – in relation to offspring outcomes [28]. In Project Viva, the mean (standard deviation) Mediterranean Diet Score (MDS) was 2.7 (1.6) out of 9 possible points; in Rhea, it was 3.8 (1.7). In each cohort, higher MDS was associated with lower BMI (Fig. 3.3).
Figure 3.3 Association of Mediterranean diet score in pregnancy with child BMI z score in (a) pooled analysis, (b) only Project Viva, and (c) only Rhea pregnancy cohort studies. Results from generalized additive models adjusted for maternal age, pre‐pregnancy body mass index, race/ethnicity, education level, parity, smoking during pregnancy, and child sex and age at outcome assessment.
From Chatzi et al. [28] © 2017 World Obesity Federation. Reproduced with permission.
In a pooled analysis, for each 3‐point increment in the MDS, offspring BMI z‐score was lower by 0.14 units (95% CI: −0.15 to −0.13), waist circumference by 0.39 cm (95% CI: −0.64 to −0.14), and the sum of skin‐fold thicknesses by 0.63 mm (95% CI: −0.98 to −0.28). In addition, higher MDS was associated with lower offspring systolic (−1.03 mmHg; 95% CI: −1.65 to −0.42) and diastolic blood pressure (−0.57 mmHg; 95% CI: −0.98 to −0.16). These results support the hypotheses that maternal adherence to the Mediterranean diet during pregnancy was associated with lower child adiposity, adipokines, and blood pressure levels.
One mechanism by which excess sugar intake and lower adherence to a Mediterranean dietary pattern might act to influence health outcomes is via increasing systemic inflammation. The Dietary Inflammatory Index (DII)™ has been developed and validated to characterize and quantify the cumulative inflammatory potential of individual diets [61]. The DII score positively correlates with interval changes in high‐sensitivity C‐reactive protein (hsCRP), a marker of systemic inflammation, in nonpregnant adults and pregnant women [61,62]. The DII is not a dietary pattern in itself but a way to assess the pro‐ or anti‐inflammatory potential of any diet. In Project Viva, dietary inflammatory index in the highest quartiles during both pregnancy and early childhood, compared to the lowest quartiles, was associated with higher waist circumference (2.4 cm; 95% CI: 0.14, 4.6) in all children and higher BMI in boys (0.78 units; 0.34, 1.22) [63]. While intervention trials are needed to confirm these associations, it seems reasonable for health care providers to recommend healthy, less inflammatory dietary patterns such as the Mediterranean diet for pregnant women.
Environmental chemicals
Recent epidemiologic and experimental data have elucidated the role of environmental chemicals on the risk for obesity and related metabolic diseases. These organic and inorganic pollutants of human and natural origin have been termed “environmental obesogens” or “metabolism‐disrupting chemicals.”
Maternal smoking during pregnancy is one well‐characterized example of an environmental exposure that appears to persistently influence offspring body weight. While prenatal smoking causes reduced fetal growth, analyses from dozens of studies have consistently found associations with later offspring obesity. One meta‐analysis of 14 studies estimated that maternal smoking during pregnancy conferred 50% increased odds (adjusted OR 1.50; 95% CI: 1.36, 1.65) for offspring obesity across an age range of 3–33 years [64]. Adjustment for factors related to social and economic position did not markedly affect estimates, and publication bias did not appear to explain the finding, but residual confounding is still possible. A more recent independent patient data meta‐analysis included 26 identified studies, including a total of 238,340 mother–child‐pairs [65]. A linear positive association was observed between the number of cigarettes smoked and offspring overweight for up to 15 cigarettes per day with an OR increased per cigarette of 1.03 (95% CI: 1.02, 1.03); the OR flattened with higher cigarette use (Fig. 3.4) [65].
A similar pattern of association as for maternal prenatal smoking, with both lower fetal growth and rapid postnatal weight gain, is seen with traffic‐related air pollution [66], supporting the smoking‐obesity relationship by analogy. Further, animal studies have observed similar findings; one in rats indicated that nicotine administration in the puerperal period led to higher adiposity through early adulthood despite no differences in maternal weight gain or size at birth [67]. Nicotine‐exposed offspring had phenotypes similar to those associated with human obesity, including higher blood pressure and impaired glucose metabolism [68,69]. Interestingly, limited data suggest that these effects may be transgenerational – F2 offspring of F1 dams exposed to nicotine during their own intrauterine development had higher blood pressure, higher fasting insulin, and greater insulin response to a glucose load [70].
Figure 3.4 Association of maternal number of cigarettes smoked per day and risk of offspring overweight (including obesity), and obesity only stratified by sex. From Albers et al. [65] ©Nature Publishing Group.
Reproduced with permission. ____ = OR for the association between maternal number of cigarettes and offspring overweight/obesity; _ _ _ = 95% CI of the OR; the vertical dashes above the x axis indicate the density of the observations underlying the model.
Per‐ and polyfluorinated substances (PFAS) are another class of chemicals that have been studied in relation to programming of obesity [71]. PFAS
