Table 2.

Outcome measures and main findings according to exposure.

Study	Outcome Measures	Main Findings
Physical activity
Antoun et al., 2020 [17]	Genome-wide DNA methylation changes in cord blood of offspring born to mothers with GDM who participated in a RCT of impact of low glycemic diet, reduced saturated fat and increased physical activity intervention during pregnancy.	No overall association between intervention and differential methylation in the cord blood. However, a total of 87% of the GDM and 77% of the 1 h glucose-associated differentially methylated CpGs had smaller effect sizes in the intervention group compared to the standard care arm.
Jönsson et al., 2021 [21]	Genome-wide DNA methylation in cord blood of offspring born to mothers participating in a RCT of impact of physical activity ± dietary intervention (low-fat and low-energy Mediterranean-style diet) in pregnancy. Also, association between intervention, methylation changes and offspring body composition.	DNA methylation was altered at 379 sites annotated to 370 genes in the intervention group versus control group (false discovery rate (FDR) < 0.05). These 370 genes are overrepresented in gene ontology terms, including response to fatty acids and adipose tissue development. Methylation of 17 sites was found to partially mediate the effect of lifestyle intervention on lean body mass in the offspring (FDR < 0.05).
Marshall et al., 2018 [4]	Association between maternal physical activity level during pregnancy and global DNA methylation as well as methylation at candidate gene level in blood from newborn. The mothers were divided into ‘high active’ (HA) and a ‘low active’ (LA).	No effect of physical activity on global DNA methylation. There were no differences between HA and LA mothers for LINE-1. However, the P2 promoter within the IGF2 gene was significantly higher in the LA group compared with HA (p = 0.045)
McCullough et al., 2015 [6]	Association between maternal non-sedentary time during pregnancy and DNA methylation at four DMRs in cord blood from offspring.	Non-sedentary time decreased methylation at the PLAG1 DMR and was found to, in part, account for an association between maternal physical activity and offspring birthweight.
Carbohydrate intake
Daniels et al., 2020 [12]	Association between DNA methylation changes at CPGs localized in the promotor region of the placenta leptin gene and maternal intake of calorie, carbohydrates, fat, protein and added sugar during pregnancy.	Lower levels of leptin methylation were associated with greater intake of carbohydrates after controlling for leptin SNP genotype (p < 0.05). Total caloric intake was also associated with placenta leptin methylation (p < 0.05), however after controlling for relevant covariates, significance diminished to trend-level. There were no associations of methylation and intake of protein (p > 0.05) or fat (p > 0.05).
Godfrey et al., 2011 [14]	Association between DNA methylation at CPGs of selected candidate genes in cord blood and maternal carbohydrate, fat and protein intake during pregnancy.	Higher methylation of RXRA chr9:136355885 was associated with lower maternal carbohydrate intake. Fat and protein intake were not associated with DNA methylation changes. Maternal intake of fat and protein were not associated with DNA methylation level.
Miyaso et al., 2017 [16]	Any association between methylation level at the H19 DMR in umbilical cord tissue and maternal diet.	Calorie intake of less than 1000 kcal/day was related to lower methylation levels at the H19 DMR (p = 0.013). The study did not find any significant effect of carbohydrate intake (OR = 1.28, p = 0.067).
Thakali et al., 2020 [22]	Association between genome-wide DNA methylation changes in placenta and maternal fat, carbohydrate, protein and saturated fat intake during pregnancy.	Maternal saturated fat intake was significantly associated with placental methylation at 302 of approximately 300,000 CpGs. Maternal carbohydrate, protein and total fat intake were significantly associated with methylation of 12, 14 and 28 CpGs, respectively. However, no maternal diet predictor variable was significantly associated with placental DNA methylation after adjusting for multiple testing.
Glycemic index
Antoun et al., 2020 [17]	See above	See above
Geraghty et al., 2018 [19]	Genome-wide DNA methylation changes in cord blood of offspring born to mothers who participated in a RCT with a low glycemic diet intervention in pregnancy.	Low glycemic intervention during pregnancy induced widespread DNA methylation changes. However, none strong enough to pass multiple testing.
Geraghty et al., 2020 [18]	Genome-wide DNA methylation changes at age 5 in offspring born to mothers who participated in a RCT with a low glycemic diet intervention in pregnancy. DNA was derived from saliva from both offspring exposed to the intervention and unexposed controls. In addition, DNA methylation and body composition at age 5 were studied.	No association was found between offspring DNA methylation and the dietary intervention in pregnancy (adjusted p < 0.05). However, applying an un-adjusted p < 0.05 identified 22,181 CPGs. The Top 1000 highest-ranking CPGs were selected for gene pathway analysis (most of them, corresponding to 60%, were hypermethylated). The gene pathway analysis showed enrichment with regards to insulin functioning.
Yan et al., 2019 [24]	Association between genome-wide DNA methylation changes in the placenta and maternal glycemic index changes during pregnancy.	Methylation levels of cg17586860 and cg18197392 in the 5ÚTR region of SSTR4 were negatively correlated with changes in carbohydrate intake and glycemic load across gestation.
Sugar intake
Daniels et al., 2020 [12]	See above	See above
Trumpff et al., 2021 [23]	Association between genome-wide DNA methylation changes in the placenta and maternal added sugar intake during pregnancy.	No individual CpGs achieved significance for altered methylation as a function of added sugar intake at each trimester or across pregnancy. A secondary analysis revealed that added sugar intake in the third trimester was associated with increased DNA methylation of a cluster of 8 CpGs within the ADD2 gene.
Mediterranean diet
Gonzalez-Nahm et al. [25]	Association between DNA methylation changes in infant cord blood leukocytes at the following DMRs: MEG3-IG, MEG3, IGF2, H19, PLAGL1, MEST, NNAT, PEG3 and SGCE/PEG10, and maternal adherence to a Mediterranean diet.	Female infants of mothers with a low adherence to a Mediterranean diet had higher odds of hypo-methylation at the MEG3-IG DMR.
Jönsson et al. [21]	See above	Se above
Fat intake
Antoun et al., 2020 [17]	See above	See above
Daniels et al., 2020 [12]	See above	See above
Godfrey et al., 2011 [14]	See above	See above
Thakali et al., 2020 [22]	See above	See above
Other exposures
Drake et al. [13]	Association between DNA methylation at CPGs localized in the GR, HSD2 and IGF2 in blood from adult offspring (40 years of age) and maternal intake of ‘an unbalanced diet’ consisting of a high meat intake and a low carbohydrate intake during pregnancy.	Offspring whose mothers reported a high meat/fish and vegetable intake combined with a low bread/potato intake had higher mean methylation at GR exon 1F. Methylation was also increased at a specific CpG site in H2D2 region 2 if the mothers had an increased meat (p = 0.03) and fish intake (p = 0.04).
Gomez Ribot et al. [20]	The relative expression of microRNA, miR-130a and miR-518d, in placenta of offspring born to mothers with GDM who participated in a RCT of the impact of three tablespoons of olive oil as a supplement to their regular diet during pregnancy.	No changes were found in the expression of miR-130a, but 518d expression was found to be increased in the placenta of GDM mothers but reduced in those GDM mothers receiving the intervention (p = 0.009).
McCullough et al., 2017 [3]	Association between methylation changes at the following DMRs: IGF2, H19, MEG3, PEG3, MEST, SGCE/PEG10, NNAT and PLAGL1 in cord blood in offspring and maternal intake of a pro-inflammatory diet during pregnancy.	No association between maternal intake of a pro-inflammatory diet and methylation of the DMRs was found.