Maternal Lifestyle Interventions: Targeting Preconception Health
Authors: Trine Moholdt, John A. Hawley
Journal: Trends in Endocrinology and Metabolism (2020)

Up to one-third of women of reproductive age are obese, predisposing their offspring to cardiometabolic diseases and initiating an intergenerational cycle of chronic metabolic disorders.Epigenetic modifications in foetal tissue play a mechanistic role in metabolic disease programming through interaction of the pregnancy environment with gene function.Primary lifestyle interventions (i.e.,diet and exercise) to improve maternal health are typically initiated in the second trimester, conferring limited benefits for mother and child.Diet–exercise interventions should commence preconception.Alternative approaches to current guidelines are urgently required to improve adherence and break the intergenerational cycle of inherited and epigenetic abnormalities of metabolism. About one-third of women of reproductive age are obese, predisposing both mother and baby to unfavourable pregnancy outcomes and initiating an intergenerational cycle of chronic metabolic disorders. Here we summarise recent research on the influence of maternal metabolic health on offspring susceptibility to future cardiometabolic diseases. Current primary lifestyle approaches (i.e., diet and exercise interventions) to halt the succession of inherited and epigenetic metabolic abnormalities have met with limited success due to late implementation, poor adherence, and/or generic guidelines. In our opinion, such interventions must commence prior to conception to improve both maternal and child health outcomes, with new approaches urgently needed to increase adherence to primary lifestyle changes among reproductive-age women. About one-third of women of reproductive age are obese, predisposing both mother and baby to unfavourable pregnancy outcomes and initiating an intergenerational cycle of chronic metabolic disorders. Here we summarise recent research on the influence of maternal metabolic health on offspring susceptibility to future cardiometabolic diseases. Current primary lifestyle approaches (i.e., diet and exercise interventions) to halt the succession of inherited and epigenetic metabolic abnormalities have met with limited success due to late implementation, poor adherence, and/or generic guidelines. In our opinion, such interventions must commence prior to conception to improve both maternal and child health outcomes, with new approaches urgently needed to increase adherence to primary lifestyle changes among reproductive-age women. Obesity and type 2 diabetes mellitus (T2D) are the biggest epidemics in human history [1.Zimmet P.Z. Diabetes and its drivers: the largest epidemic in human history?.Clin. Diabetes Endocrinol. 2017; 3: 1Crossref PubMed Scopus (121) Google Scholar] and the major challenge to health-care systems worldwide in the 21st century. Compared with 20 years ago, twice as many people are diagnosed with T2D, and the rapid increase in obesity and T2D among children, adolescents, and young adults predisposes future generations to increased risk for numerous chronic diseases [2.Zimmet P.Z. et al.Diabetes: a 21st century challenge.Lancet Diabetes Endocrinol. 2014; 2: 56-64Abstract Full Text Full Text PDF PubMed Scopus (431) Google Scholar]. Obesity is the result of complex interactions between genetic, environmental, and socioeconomic influences. While family history is a strong determinant for both obesity and T2D, genome-wide estimates suggest that only ~20% of obesity and T2D risk is attributable to fixed genomic variation [3.Locke A.E. et al.Genetic studies of body mass index yield new insights for obesity biology.Nature. 2015; 518: 197-206Crossref PubMed Scopus (2134) Google Scholar,4.Mahajan A. et al.Fine-mapping type 2 diabetes loci to single-variant resolution using high-density imputation and islet-specific epigenome maps.Nat. Genet. 2018; 50: 1505-1513Crossref PubMed Scopus (405) Google Scholar], leaving a large part of heritability unexplained. Behavioural and environmental factors influence patterns of gene expression via gene–environment interactions and epigenetic modifications (see Glossary) and provide a molecular basis for the 'missing' heritability associated with the elevated risk for obesity and T2D [5.Barres R. Zierath J.R. The role of diet and exercise in the transgenerational epigenetic landscape of T2DM.Nat. Rev. Endocrinol. 2016; 12: 441-451Crossref PubMed Scopus (94) Google Scholar]. In support of this premise, robust associations exist between susceptibility to life-long obesity, impaired glucose tolerance (IGT), and T2D in offspring and epigenetic modifications, confirming that metabolic dysfunction is transmitted across generations [6.Jaeger K. et al.Transmission of metabolic dysfunction across generations.Physiology (Bethesda). 2017; 32: 51-59Crossref PubMed Scopus (17) Google Scholar]. The importance of early human embryonic and foetal life for later increased risk of metabolic disturbances is captured in the Developmental Origins of Health and Disease (DOHaD) hypothesis [7.Gluckman P.D. et al.A conceptual framework for the developmental origins of health and disease.J. Dev. Orig. Health Dis. 2010; 1: 6-18Crossref PubMed Scopus (188) Google Scholar]. Maternal lifestyle prior to and during pregnancy is, therefore, of paramount importance for the epigenetic mapping of the offspring [5.Barres R. Zierath J.R. The role of diet and exercise in the transgenerational epigenetic landscape of T2DM.Nat. Rev. Endocrinol. 2016; 12: 441-451Crossref PubMed Scopus (94) Google Scholar] and underpins the intergenerational cycle of obesity, insulin resistance, and associated disorders (Figure 1). Maternal overweight and obesity are associated with a substantially higher risk of gestational diabetes mellitus (GDM) [8.Chu S.Y. et al.Maternal obesity and risk of gestational diabetes mellitus.Diabetes Care. 2007; 30: 2070-2076Crossref PubMed Scopus (616) Google Scholar]. Both environmental factors and genetics contribute to the development of GDM, with up to 14% of live births negatively impacted by this condition [9.Ogurtsova K. et al.IDF Diabetes Atlas: global estimates for the prevalence of diabetes for 2015 and 2040.Diabetes Res. Clin. Pract. 2017; 128: 40-50Abstract Full Text Full Text PDF PubMed Scopus (1645) Google Scholar]. Both maternal obesity and GDM are independently associated with adverse pregnancy outcomes and their combination has a greater impact than either one alone [10.Catalano P.M. et al.The hyperglycemia and adverse pregnancy outcome study: associations of GDM and obesity with pregnancy outcomes.Diabetes Care. 2012; 35: 780-786Crossref PubMed Scopus (549) Google Scholar]. Maternal glucose intolerance in GDM results from peripheral insulin resistance and the failure of β-cell compensation and maternal insulin production to cope with the prevailing hyperglycaemia. Maternal glucose crosses the maternoembryonic interface, but insulin does not, leading to foetal hyperglycaemia, hyperinsulinaemia, and a vicious cycle of low-grade inflammation. Offspring exposed to untreated GDMin utero are insulin resistant with limited β-cell compensation compared with offspring of mothers with normal glycaemia during pregnancy [11.Lowe Jr., W.L. et al.Hyperglycemia and Adverse Pregnancy Outcome Follow-up Study (HAPO FUS): maternal gestational diabetes mellitus and childhood glucose metabolism.Diabetes Care. 2019; 42: 372-380Crossref PubMed Scopus (118) Google Scholar]. GDM is independently associated with childhood IGT [11.Lowe Jr., W.L. et al.Hyperglycemia and Adverse Pregnancy Outcome Follow-up Study (HAPO FUS): maternal gestational diabetes mellitus and childhood glucose metabolism.Diabetes Care. 2019; 42: 372-380Crossref PubMed Scopus (118) Google Scholar] and exposure to hyperglycaemia in utero is strongly related to childhood adiposity, including overweight/obesity, increased skinfold thickness and body fat, and greater waist circumference [12.Lowe Jr., W.L. et al.Maternal glucose levels during pregnancy and childhood adiposity in the Hyperglycemia and Adverse Pregnancy Outcome Follow-up Study.Diabetologia. 2019; 62: 598-610Crossref PubMed Scopus (56) Google Scholar]. Even glucose concentrations lower than those diagnostic of GDM are associated with increased birth weight and elevated levels of cord-bloodC-peptide (reflective of the insulin-secretory activity of pancreatic β-cells, which modulates foetal growth), greater childhood adiposity, and elevated blood pressure, independent of maternal body mass index (BMI) [12.Lowe Jr., W.L. et al.Maternal glucose levels during pregnancy and childhood adiposity in the Hyperglycemia and Adverse Pregnancy Outcome Follow-up Study.Diabetologia. 2019; 62: 598-610Crossref PubMed Scopus (56) Google Scholar, 13.Grunnet L.G. et al.Adiposity, dysmetabolic traits, and earlier onset of female puberty in adolescent offspring of women with gestational diabetes mellitus: a clinical study within the Danish National Birth Cohort.Diabetes Care. 2017; 40: 1746-1755Crossref PubMed Scopus (44) Google Scholar, 14.Tam W.H. et al.In utero exposure to maternal hyperglycemia increases childhood cardiometabolic risk in offspring.Diabetes Care. 2017; 40: 679-686Crossref PubMed Scopus (125) Google Scholar]. Foetal exposure to maternal GDM programmes future risk of obesity, IGT, T2D, and cardiovascular disease [11.Lowe Jr., W.L. et al.Hyperglycemia and Adverse Pregnancy Outcome Follow-up Study (HAPO FUS): maternal gestational diabetes mellitus and childhood glucose metabolism.Diabetes Care. 2019; 42: 372-380Crossref PubMed Scopus (118) Google Scholar, 12.Lowe Jr., W.L. et al.Maternal glucose levels during pregnancy and childhood adiposity in the Hyperglycemia and Adverse Pregnancy Outcome Follow-up Study.Diabetologia. 2019; 62: 598-610Crossref PubMed Scopus (56) Google Scholar, 13.Grunnet L.G. et al.Adiposity, dysmetabolic traits, and earlier onset of female puberty in adolescent offspring of women with gestational diabetes mellitus: a clinical study within the Danish National Birth Cohort.Diabetes Care. 2017; 40: 1746-1755Crossref PubMed Scopus (44) Google Scholar, 14.Tam W.H. et al.In utero exposure to maternal hyperglycemia increases childhood cardiometabolic risk in offspring.Diabetes Care. 2017; 40: 679-686Crossref PubMed Scopus (125) Google Scholar, 15.Reynolds R.M. et al.Maternal obesity during pregnancy and premature mortality from cardiovascular event in adult offspring: follow-up of 1 323 275 person years.BMJ. 2013; 347: f4539Crossref PubMed Scopus (290) Google Scholar, 16.Lowe Jr., W.L. et al.Association of gestational diabetes with maternal disorders of glucose metabolism and childhood adiposity.JAMA. 2018; 320: 1005-1016Crossref PubMed Scopus (159) Google Scholar]. Thus, epigenetic modifications in foetal tissue play a mechanistic role in metabolic disease programming through the interaction of the pregnancy environment with gene function. Such epigenetic modifications can occur via DNA methylation, histone modification, and/or alterations to noncoding RNAs. Evidence supporting a role for hyperglycaemia-induced changes in the pattern of DNA methylation comes from studies of maternal and offspring cord blood. Kang et al. [17.Kang J. et al.Genome-wideDNA methylation variation in maternal and cord blood of gestational diabetes population.Diabetes Res. Clin. Pract. 2017; 132: 127-136Abstract Full Text Full Text PDF PubMed Scopus (28) Google Scholar] collected maternal andcord blood samples from 16 pregnant women and their newborns, including eight exposed to GDM. They identified 200 loci and their corresponding genes in the maternal and cord blood that were differently methylated in women with GDM compared with women who were normoglycaemic. Bouchard et al. [18.Bouchard L. et al.Leptin gene epigenetic adaptation to impaired glucose metabolism during pregnancy.Diabetes Care. 2010; 33: 2436-2441Crossref PubMed Scopus (166) Google Scholar] found significant correlations between 2-h glucose concentrations after an oral glucose tolerance test and the degree of DNA methylation of the leptin gene in placenta on both the foetal and maternal side in women with GDM: higher glucose values correlated with a lower magnitude of methylation on the foetal side, but with a higher degree of methylation (and repression of gene transcription) on the maternal side. No such maternal–foetal pattern of methylation was found in healthy pregnant women.Others have identified multiple genome-wide differences in DNA methylation in foetal tissues from mothers with GDM versus healthy controls [19.Moen G.H. et al.Mechanisms in endocrinology: epigenetic modifications and gestational diabetes: a systematic review of published literature.Eur. J. Endocrinol. 2017; 176: R247-R267Crossref PubMed Scopus (26) Google Scholar]. However, we currently have limited knowledge about the clinical relevance of these findings as most studies have been limited by small sample sizes and adjusted for few covariates. The process of histone acetylation regulates many cellular functions, with dysregulation of histone modification being an important factor in the pathophysiology of metabolic diseases and foetal programming. Studies of the impact of maternal obesity and GDM on histone modification are few, however, and this is a fertile area for future research. By contrast, there are extensive reports of the impact of GDM on noncoding miRNAs and their gene targets [19.Moen G.H. et al.Mechanisms in endocrinology: epigenetic modifications and gestational diabetes: a systematic review of published literature.Eur. J. Endocrinol. 2017; 176: R247-R267Crossref PubMed Scopus (26) Google Scholar]. Zhu et al. [20.Zhu Y. et al.Profiling maternal plasma microRNA expression in early pregnancy to predict gestational diabetes mellitus.Int. J. Gynaecol. Obstet. 2015; 130: 49-53Crossref PubMed Scopus (81) Google Scholar] profiled the expression of plasma miRNAs in mothers with GDM and healthy controls and found 32miRNAs that were differentially expressed, with the targets of these miRNAs associated with insulin resistance and poor pregnancy outcomes (i.e., preeclampsia, emergency Caesarean section, and neonatal hypoglycaemia). A study on placentas from women with either dietary controlled GDM or GDM controlled by medication and from matched controls found differential expression of miRNAs whose targets involved mitochondrial function and glucose metabolism [21.Muralimanoharan S. et al.Mitochondrial function and glucose metabolism in the placenta with gestational diabetes mellitus: role of miR-143.Clin. Sci. (Lond.). 2016; 130: 931-941Crossref PubMed Scopus (72) Google Scholar]. In that study, lower protein levels of the transcriptional coactivator peroxisome proliferator-activated receptor gamma coactivator1 alpha (PGC1-α) were observed in both GDM groups compared with BMI-matched controls. Epigenetic modifications have their origin in poor preconception and maternal lifestyle choices with such cues exacerbating any pre-existing abnormalities in metabolism: unfavourable dietary practices combined with insufficient physical activity increase the risk of GDM-related complications. In this context, we define 'preconception' as the weeks or months from a conscious intention to conceive until conception, but acknowledge that preconception risk factors such as poor dietary quality, lack of regular physical activity, and obesity should be addressed over the preceding months and years. Diet (quality and energy content) affects multiple facets of human health and is inextricably linked to many chronic metabolic conditions. Maternal diet contributes to a foetal 'epigenetic signature' that impacts individual susceptibility to disease risk in the offspring later in life [22.Li Y. Epigenetic mechanisms link maternal diets and gut microbiome to obesity in the offspring.Front. Genet. 2018; 9: 342Crossref PubMed Scopus (44) Google Scholar,23.Tamburini S. et al.The microbiome in early life: implications for health outcomes.Nat. Med. 2016; 22: 713-722Crossref PubMed Scopus (437) Google Scholar]. Diet causes profound changes in gut microbiota in pregnancy and affects the gut microbiota in newborns [24.Calatayud M. et al.Maternal microbiome and metabolic health program microbiome development and health of the offspring.Trends Endocrinol. Metab. 2019; 30: 735-744Abstract Full Text Full Text PDF PubMed Scopus (21) Google Scholar]. The initial development and maturation of the neonatal microbiota is largely determined by maternal–offspring exchanges of microbiota. An altered gut microbiota also directly influences immune cells in the gut and indirectly affects immune cells via microbial products (e.g.,lipopolysaccharides, short-chain fatty acids), impacting adipogenesis and/or insulin resistance [25.Cani P.D. et al.Involvement of gut microbiota in the development of low-grade inflammation and type 2 diabetes associated with obesity.Gut Microbes. 2012; 3: 279-288Crossref PubMed Scopus (449) Google Scholar]. Crusell et al. [26.Crusell M.K.W. et al.Gestational diabetes is associated with change in the gut microbiota composition in third trimester of pregnancy and postpartum.Microbiome. 2018; 6: 89Crossref PubMed Scopus (120) Google Scholar] assessed the gut microbiota composition of women with GDM in the third trimester of pregnancy and found a disrupted gut microbiota composition compared with normoglycaemic pregnant women. Differences in 'microbiota signatures' were still evident 8 months postpartum. They concluded that the composition of the gut microbiota from women with GDM, both during and after pregnancy, resembled the aberrant microbiota composition reported in non-pregnant individuals with T2D [26.Crusell M.K.W. et al.Gestational diabetes is associated with change in the gut microbiota composition in third trimester of pregnancy and postpartum.Microbiome. 2018; 6: 89Crossref PubMed Scopus (120) Google Scholar]. Since a growing body of evidence suggests that the period from conception through the first 2 years of life is pivotal for the formation of the gut microbiota, maternal preconception and early pregnancy present a unique opportunity to modify the composition of the gut bacteria of both mother and offspring [24.Calatayud M. et al.Maternal microbiome and metabolic health program microbiome development and health of the offspring.Trends Endocrinol. Metab. 2019; 30: 735-744Abstract Full Text Full Text PDF PubMed Scopus (21) Google Scholar]. The 2018 Lancet series on preconception maternal health focused scientific and media attention on the health and wellbeing of women at the time of conception, highlighting this critical period forshaping pregnancy outcomes and future maternal and child health [27.Stephenson J. et al.Before the beginning: nutrition and lifestyle in the preconception period and its importance for future health.Lancet. 2018; 391: 1830-1841Abstract Full Text Full Text PDF PubMed Scopus (306) Google Scholar, 28.Fleming T.P. et al.Origins of lifetime health around the time of conception: causes and consequences.Lancet. 2018; 391: 1842-1852Abstract Full Text Full Text PDF PubMed Scopus (317) Google Scholar, 29.Barker M. et al.Intervention strategies to improve nutrition and health behaviours before conception.Lancet. 2018; 391: 1853-1864Abstract Full Text Full Text PDF PubMed Scopus (129) Google Scholar]. The government in the UK reacted swiftly to this message, producing resources to raise public awareness on preconception care [30.Stephenson J. et al.Preconception health in England: a proposal for annual reporting with core metrics.Lancet. 2019; 393: 2262-2271Abstract Full Text Full Text PDF PubMed Scopus (21) Google Scholar]. Such initiatives are to be applauded. However, there were grounds for concern. First was the limited scope of preconception strategies, with emphasis placed almost exclusively on 'improving the food environment' and little or no mention of physical activity/exercise training as a major lifestyle intervention to enhance whole-body metabolic health. Second, the scale of the initiatives was wideranging, lacking specific prescriptive recommendations that many pregnant women seek. There is limited evidence that current dietary approaches have any clinically meaningful effect on pregnancy outcomes for either the mother or the infant among women who are overweight/obese or who have already developed GDM [31.Tieu J. et al.Dietary advice interventions in pregnancy for preventing gestational diabetes mellitus.Cochrane Database Syst. Rev. 2017; 1CD006674PubMed Google Scholar,32.Martis R. et al.Treatments for women with gestational diabetes mellitus: an overview of Cochrane systematic reviews.Cochrane Database Syst. Rev. 2018; 8CD012327PubMed Google Scholar]. Results from the majority of clinical trials show that dietary interventions are ineffective in preventing GDM [31.Tieu J. et al.Dietary advice interventions in pregnancy for preventing gestational diabetes mellitus.Cochrane Database Syst. Rev. 2017; 1CD006674PubMed Google Scholar]. There is insufficient evidence to support any single dietary intervention to offset the deleterious effects of GDM in women who already have developed this condition [32.Martis R. et al.Treatments for women with gestational diabetes mellitus: an overview of Cochrane systematic reviews.Cochrane Database Syst. Rev. 2018; 8CD012327PubMed Google Scholar]. By contrast, preconception adherence to healthy dietary habits is associated with a lower risk of GDM [33.Tobias D.K. et al.Prepregnancy adherence to dietary patterns and lower risk of gestational diabetes mellitus.Am. J. Clin. Nutr. 2012; 96: 289-295Crossref PubMed Scopus (107) Google Scholar], supporting the premise that lifestyle modification should commence before pregnancy. It is clear that merely providing women with information about dietary guidelines before or during pregnancy is totally inadequate to reduce the clinical risks associated with poor maternal metabolic health [31.Tieu J. et al.Dietary advice interventions in pregnancy for preventing gestational diabetes mellitus.Cochrane Database Syst. Rev. 2017; 1CD006674PubMed Google Scholar,32.Martis R. et al.Treatments for women with gestational diabetes mellitus: an overview of Cochrane systematic reviews.Cochrane Database Syst. Rev. 2018; 8CD012327PubMed Google Scholar]. Regarding physical activity, European and American guidelines advocate that women should accumulate ≥150 min/week of moderate-intensity exercise (e.g.,30min of brisk walking on at least 5 days of the week) during pregnancy to help control healthy gestational weight gain and prevent GDM [34.ACOG ACOG Committee Opinion No. 650: physical activity and exercise during pregnancy and the postpartum period.Obstet. 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Randomised controlled trials with a focus on exercise training in overweight/obese women during pregnancy consistently report disappointing outcomes, with little effect of exercise on maternal glycaemic control, gestational weight gain, and/or infant outcomes [37.Poston L. et al.Effect of a behavioural intervention in obese pregnant women (the UPBEAT study): a multicentre, randomised controlled trial.Lancet Diabetes Endocrinol. 2015; 3: 767-777Abstract Full Text Full Text PDF PubMed Scopus (366) Google Scholar, 38.Rono K. et al.Effect of a lifestyle intervention during pregnancy – findings from the Finnish gestational diabetes prevention trial (RADIEL).J. 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The exercise prescription in most studies encompasses 2–3 h of weekly moderate-intensity training, but <50% of women adhere to such protocols [41.Garnaes K.K. et al.Exercise training and weight gain in obese pregnant women: a randomized controlled trial (ETIP Trial).PLoS Med. 2016; 13e1002079Crossref PubMed Scopus (62) Google Scholar,42.Seneviratne S.N. et al.Effects of antenatal exercise in overweight and obese pregnant women on maternal and perinatal outcomes: a randomised controlled trial.BJOG. 2016; 123: 588-597Crossref PubMed Scopus (51) Google Scholar]. Barriers to physical activity during pregnancy include 'a lack of time','having other children', a 'lack of knowledge', and, importantly, being unclear on what type of exercise is safe to undertake [43.Flannery C. et al.Enablers and barriers to physical activity in overweight and obese pregnant women: an analysis informed by the theoretical domains framework and COM-B model.BMC Pregnancy Childbirth. 2018; 18: 178Crossref PubMed Scopus (32) Google Scholar]. Of note, patterns of pre-pregnancy physical activity is an important determinant of exercise habits during pregnancy [44.Gaston A. Cramp A. Exercise during pregnancy: a review of patterns and determinants.J. Sci. Med. Sport. 2011; 14: 299-305Abstract Full Text Full Text PDF PubMed Scopus (163) Google Scholar]. Therefore, exercise habits need to be established early, with alternative, practical strategies to current guidelines urgently needed to increase adherence. Pregnancy is regarded as a 'teachable moment' to instil lifestyle changes, with previously inactive women being strongly encouraged to be physically active throughout pregnancy[45.Mottola M.F. et al.2019 Canadian guideline for physical activity throughout pregnancy.Br. J. Sports Med. 2018; 52: 1339-1346Crossref PubMed Scopus (139) Google Scholar]. Still, we argue that it is too little and too late to initiate major lifestyle reforms during gestation. Perhaps more to the point, commencing primary lifestyle interventions much earlier will have a greater impact on maternal and offspring health outcomes [46.Catalano P. deMouzon S.H. Maternal obesity and metabolic risk to the offspring: why lifestyle interventions may have not achieved the desired outcomes.Int. J. Obes. 2015; 39: 642-649Crossref PubMed Scopus (135) Google Scholar]. In this regard, enhancing preconception health is a challenging proposition with vast potential for improvement [30.Stephenson J. et al.Preconception health in England: a proposal for annual reporting with core metrics.Lancet. 2019; 393: 2262-2271Abstract Full Text Full Text PDF PubMed Scopus (21) Google Scholar]. Notwithstanding this challenge, the main goal of any intervention should be to induce rapid enhancements in maternal insulin sensitivity. Weight loss should not be the primary goal, since most women planning a pregnancy will aim to get pregnant in a time-frame too short for substantial weight reduction. Specific diet–exercise strategies to improve insulin sensitivity are needed for women who are planning a pregnancy and these should be implemented alongside continued efforts to reverse the obesity epidemic at a population level. Below we outline two complementary primary lifestyle interventions to be initiated prior to and continued throughout pregnancy. We believe these strategies are feasible and practical and will help to break the intergenerational cycle of chronic metabolic disease states (Figure 2). Epidemiological data demonstrate that the quality and quantity of food consumed are directly linked to human health, with current population nutrition guidelines as well as those for pregnant women emphasising food-based recommendations (i.e., the combinations and quantities of foods and nutrients consumed) as important determinants of metabolic health [47.Kaiser L.L. Allen L. Position of the American Dietetic Association: nutrition and lifestyle for a healthy pregnancy outcome.J. Am. Diet. Assoc. 2002; 102: 1479-1490Abstract Full Text Full Text PDF PubMed Scopus (122) Google Scholar]. However, contemporary position stands make no mention of the timing of food intake during the day, which is critical for the wellbeing of an organism [48.Melkani G.C. Panda S. Time-restricted feeding for prevention and treatment of cardiometabolic disorders.J. Physiol. 2017; 595: 3691-3700Crossref PubMed Scopus (74) Google Scholar]. Objective data of the eating behaviours of women before or during pregnancy are limited [49.Bailey R.L. et al.Estimation of total usual dietary intakes of pregnant women in the United States.JAMA Netw. Open. 2019; 2e195967Crossref PubMed Scopus (40) Google Scholar], but recent technological advances have made it possible to capture real-time information on free-living eating patterns in humans. Gill and Panda [50.Gill S. Panda S. A smartphone app reveals erratic diurnal eating patterns in humans that can be modulated for health benefits.Cell Metab. 2015; 22: 789-798Abstract Full Text Full Text PDF PubMed Scopus (316) Google Scholar] monitored 156 adults with overweight/obesity for 3 weeks and reported that the time from the first energy intake of the day to the final eating occasion was ~15 h. There was a bias toward eating late, which was associated with reduced dietary qualit