Nicole E. Marshall

Dr. Nicole E. Marshall


Research Focus & Metrics

Academic Career Length

16Years (2011-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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27 December 2021 in American Journal of Obstetrics and Gynecology
Verified
Journal Article
Open access
NMNicole E. Marshall
Nicole E. Marshall
BABarbara Abrams
Barbara Abrams
LBLinda A. Barbour
Linda A. Barbour
PCPatrick Catalano
Patrick Catalano
PCParul Christian
Parul Christian
KTKent L. Thornburg
Kent L. Thornburg
Most women in the United States do not meet the recommendations for healthful nutrition and weight before and during pregnancy. Women and providers often ask what a healthy diet for a pregnant woman should look like. The message should be “eat better, not more.” This can be achieved by basing diet on a variety of nutrient-dense, whole foods, including fruits, vegetables, legumes, whole grains, healthy fats with omega-3 fatty acids that include nuts and seeds, and fish, in place of poorer quality highly processed foods. Such a diet embodies nutritional density and is less likely to be accompanied by excessive energy intake than the standard American diet consisting of increased intakes of processed foods, fatty red meat, and sweetened foods and beverages. Women who report “prudent” or “health-conscious” eating patterns before and/or during pregnancy may have fewer pregnancy complications and adverse child health outcomes. Comprehensive nutritional supplementation (multiple micronutrients plus balanced protein energy) among women with inadequate nutrition has been associated with improved birth outcomes, including decreased rates of low birthweight. A diet that severely restricts any macronutrient class should be avoided, specifically the ketogenic diet that lacks carbohydrates, the Paleo diet because of dairy restriction, and any diet characterized by excess saturated fats. User-friendly tools to facilitate a quick evaluation of dietary patterns with clear guidance on how to address dietary inadequacies and embedded support from trained healthcare providers are urgently needed.

1 September 2011 in American Journal of Obstetrics and Gynecology
Verified
Journal Article
Closed access
NMNicole E. Marshall
Nicole E. Marshall
RFRongwei Fu
Rongwei Fu
JGJeanne-Marie Guise
Jeanne-Marie Guise

1 May 2012 in American Journal of Obstetrics and Gynecology
Verified
Journal Article
Closed access
NMNicole E. Marshall
Nicole E. Marshall
CGCamelia Guild
Camelia Guild
YCYvonne W. Cheng
Yvonne W. Cheng
ACAaron B. Caughey
Aaron B. Caughey
DHDonna R. Halloran
Donna R. Halloran

21 October 2018 in Maternal & Child Nutrition
Verified
Journal Article
Closed access
PDF file
NMNicole E. Marshall
Nicole E. Marshall
BLBernard Lau
Bernard Lau
JPJonathan Q. Purnell
Jonathan Q. Purnell
KTKent L. Thornburg
Kent L. Thornburg

15 October 2017 in The Journal of Immunology
Verified
Journal Article
Closed access
PDF file
SSSuhas Sureshchandra
Suhas Sureshchandra
RWRandall M. Wilson
Randall M. Wilson
MRMaham Rais
Maham Rais
NMNicole E. Marshall
Nicole E. Marshall
JPJonathan Q. Purnell
Jonathan Q. Purnell
IMIlhem Messaoudi
Ilhem Messaoudi
Prepregnancy maternal obesity is associated with adverse outcomes for the offspring, including increased incidence of neonatal bacterial sepsis and necrotizing enterocolitis. We recently reported that umbilical cord blood (UCB) monocytes from babies born to obese mothers generate a reduced IL-6/TNF-α response to TLR 1/2 and 4 ligands compared to those collected from lean mothers. These observations suggest altered development of the offspring’s immune system, which in turn results in dysregulated function. We therefore investigated transcriptional and epigenetic differences within UCB monocytes stratified by prepregnancy maternal body mass index. We show that UCB monocytes from babies born to obese mothers generate a dampened response to LPS stimulation compared with those born to lean mothers, at the level of secreted immune mediators and transcription. Because gene expression profiles of resting UCB monocytes from both groups were comparable, we next investigated the role of epigenetic differences. Indeed, we detected stark differences in methylation levels within promoters and regulatory regions of genes involved in TLR signaling in resting UCB monocytes. Interestingly, the DNA methylation status of resting cells was highly predictive of transcriptional changes post-LPS stimulation, suggesting that cytosine methylation is one of the dominant mechanisms driving functional inadequacy in UCB monocytes obtained from babies born to obese mothers. These data highlight a potentially critical role of maternal pregravid obesity-associated epigenetic changes in influencing the function of an offspring’s monocytes at birth. These findings further our understanding of mechanisms that explain the increased risk of infection in neonates born to mothers with high prepregnancy body mass index.

6 October 2018 in American Journal of Perinatology
Verified
Journal Article
Closed access
PDF file
NMNicole E. Marshall
Nicole E. Marshall
FBFrances M. Biel
Frances M. Biel
JBJanne Boone-Heinonen
Janne Boone-Heinonen
DDDmitry Dukhovny
Dmitry Dukhovny
ACAaron B. Caughey
Aaron B. Caughey
JSJonathan M. Snowden
Jonathan M. Snowden
Objective To test the hypothesis that maternal height is associated with adverse perinatal outcomes, controlling for and stratified by maternal body mass index (BMI). Study Design This was a retrospective cohort study of all births in California between 2007 and 2010 (n = 1,775,984). Maternal height was categorized into quintiles, with lowest quintile (≤20%) representing shorter stature and the uppermost quintile (≥80%) representing taller stature. Outcomes included gestational diabetes mellitus (GDM), preeclampsia, cesarean, preterm birth (PTB), macrosomia, and low birth weight (LBW). We calculated height/outcome associations among BMI categories, and BMI/outcome associations among height categories, using various multivariable logistic regression models. Results Taller women were less likely to have GDM, nulliparous cesarean, PTB, and LBW; these associations were similar across maternal BMI categories and persisted after multivariable adjustment. In contrast, when stratified by maternal height, the associations between maternal BMI and birth outcomes varied by specific outcomes, for example, the association between morbid obesity (compared with normal or overweight) and the risk of GDM was weaker among shorter women (adjusted odds ratio [aOR], 95% confidence interval [CI]: 3.48, 3.28–3.69) than taller women (aOR, 95% CI: 4.42, 4.19–4.66). Conclusion Maternal height is strongly associated with altered perinatal risk even after accounting for variations in complications by BMI.