Dates of Funding: 2022-2024
I am a Post-doctoral Fellow in the Department of Pediatrics, Section of Nutrition at the University of Colorado – Anschutz Medical Center, supported by the Ruth L. Kirschstein National Research Service Award T32 Research Fellowship in Nutrition at the University of Colorado – Anschutz Medical Campus (CU – Anschutz). My research interest is in understanding the interactions of nutrition, maternal intrauterine exposures, and epigenetics on obesity risk in childhood. My long-term career goal is to establish myself as an independent physician scientist critically assessing the most optimal nutritional strategies for children at high risk of obesity and associated co-morbidities in the context of their interaction with genetic predisposition, susceptibility conferred via intrauterine exposures, and their effects on infant and child growth.  My interests lie in understanding the how the totality of these exposures and potential predictors can be moderated by evidence based nutritional interventions established earlier and sustained throughout the life course. 

Differences in childhood obesity risk may appear in infancy, suggesting that factors driving obesity begin operating very early in life. Neural, metabolic, and hormonal networks regulating energy balance are established in utero and are likely influenced by maternal exposures, including nutrition. Human studies have shown that such networks may be determined by epigenetic modifications, of which DNA methylation is the most well studied to date. Studies also indicate that maternal one carbon (1C) nutrient intake, such as that of folate and choline, peri-conceptionally and during pregnancy can influence both offspring adiposity and DNA methylation. Few studies, however, have aimed to evaluate the mediation of adiposity risk by DNA methylation in relation to its association with maternal 1C nutrient concentrations.  Differential DNA methylation, influenced by maternal 1C nutrient status, may serve as a marker at birth that predicts risk of adiposity, informing the need for additional clinical monitoring or alternative nutritional recommendations to prevent exacerbated growth.

For my NORC pilot award I propose to determine whether intrauterine exposure to maternal concentrations of folate and choline through 27 weeks gestation influences offspring adiposity and is mediated by DNA methylation identified at birth by leveraging data obtained from the Healthy Start Study (R01 DK076648, PI: Dabelea) an ongoing a large, multi-ethnic, prebirth cohort that has collected DNA methylation at birth in ~600 infants and longitudinal adiposity measures at birth, 5 months, and 5 years of age in the offspring.  More specifically, in this population of mother-infant dyads in which maternal intake of these two 1-carbon nutrient precursors is outside of recommended intake ranges during pregnancy, I aim to 1) precisely elucidate the effect of excessive folate status and inadequate choline status, based on maternal serum concentrations, on infant and child adiposity outcomes, and 2) examine mediation by DNA methylation in offspring cord blood.  Our results will contribute to knowledge and may clarify rising concerns regarding “population wide excess folate status” especially in pregnant women due to dose exposure and the potential for long term adverse effects on offspring health. This investigation will also indicate whether such status has any potential compensatory effect on offspring anthropometric outcomes or DNA methylation in the context of low choline concentrations amongst the population of maternal-infant dyads studied.  Additionally, the NORC award will facilitate my career goals of obtaining a future career development grant and establishing independently funded research.

Dates of Funding: 2022-2024
I am a Post-doctoral Fellow in the Department of Pediatrics, Section of Nutrition at the University of Colorado – Anschutz Medical Center, supported by the Ruth L. Kirschstein National Research Service Award T32 Research Fellowship in Nutrition at the University of Colorado – Anschutz Medical Campus (CU – Anschutz). My research interest is in understanding the interactions of nutrition, maternal intrauterine exposures, and epigenetics on obesity risk in childhood. My long-term career goal is to establish myself as an independent physician scientist critically assessing the most optimal nutritional strategies for children at high risk of obesity and associated co-morbidities in the context of their interaction with genetic predisposition, susceptibility conferred via intrauterine exposures, and their effects on infant and child growth.  My interests lie in understanding the how the totality of these exposures and potential predictors can be moderated by evidence based nutritional interventions established earlier and sustained throughout the life course. 

Differences in childhood obesity risk may appear in infancy, suggesting that factors driving obesity begin operating very early in life. Neural, metabolic, and hormonal networks regulating energy balance are established in utero and are likely influenced by maternal exposures, including nutrition. Human studies have shown that such networks may be determined by epigenetic modifications, of which DNA methylation is the most well studied to date. Studies also indicate that maternal one carbon (1C) nutrient intake, such as that of folate and choline, peri-conceptionally and during pregnancy can influence both offspring adiposity and DNA methylation. Few studies, however, have aimed to evaluate the mediation of adiposity risk by DNA methylation in relation to its association with maternal 1C nutrient concentrations.  Differential DNA methylation, influenced by maternal 1C nutrient status, may serve as a marker at birth that predicts risk of adiposity, informing the need for additional clinical monitoring or alternative nutritional recommendations to prevent exacerbated growth.

For my NORC pilot award I propose to determine whether intrauterine exposure to maternal concentrations of folate and choline through 27 weeks gestation influences offspring adiposity and is mediated by DNA methylation identified at birth by leveraging data obtained from the Healthy Start Study (R01 DK076648, PI: Dabelea) an ongoing a large, multi-ethnic, prebirth cohort that has collected DNA methylation at birth in ~600 infants and longitudinal adiposity measures at birth, 5 months, and 5 years of age in the offspring.  More specifically, in this population of mother-infant dyads in which maternal intake of these two 1-carbon nutrient precursors is outside of recommended intake ranges during pregnancy, I aim to 1) precisely elucidate the effect of excessive folate status and inadequate choline status, based on maternal serum concentrations, on infant and child adiposity outcomes, and 2) examine mediation by DNA methylation in offspring cord blood.  Our results will contribute to knowledge and may clarify rising concerns regarding “population wide excess folate status” especially in pregnant women due to dose exposure and the potential for long term adverse effects on offspring health. This investigation will also indicate whether such status has any potential compensatory effect on offspring anthropometric outcomes or DNA methylation in the context of low choline concentrations amongst the population of maternal-infant dyads studied.  Additionally, the NORC award will facilitate my career goals of obtaining a future career development grant and establishing independently funded research.

Dates of Funding: 2022-2024
I am a Post-doctoral Fellow in the Department of Pediatrics, Section of Nutrition at the University of Colorado – Anschutz Medical Center, supported by the Ruth L. Kirschstein National Research Service Award T32 Research Fellowship in Nutrition at the University of Colorado – Anschutz Medical Campus (CU – Anschutz). My research interest is in understanding the interactions of nutrition, maternal intrauterine exposures, and epigenetics on obesity risk in childhood. My long-term career goal is to establish myself as an independent physician scientist critically assessing the most optimal nutritional strategies for children at high risk of obesity and associated co-morbidities in the context of their interaction with genetic predisposition, susceptibility conferred via intrauterine exposures, and their effects on infant and child growth.  My interests lie in understanding the how the totality of these exposures and potential predictors can be moderated by evidence based nutritional interventions established earlier and sustained throughout the life course. 

Differences in childhood obesity risk may appear in infancy, suggesting that factors driving obesity begin operating very early in life. Neural, metabolic, and hormonal networks regulating energy balance are established in utero and are likely influenced by maternal exposures, including nutrition. Human studies have shown that such networks may be determined by epigenetic modifications, of which DNA methylation is the most well studied to date. Studies also indicate that maternal one carbon (1C) nutrient intake, such as that of folate and choline, peri-conceptionally and during pregnancy can influence both offspring adiposity and DNA methylation. Few studies, however, have aimed to evaluate the mediation of adiposity risk by DNA methylation in relation to its association with maternal 1C nutrient concentrations.  Differential DNA methylation, influenced by maternal 1C nutrient status, may serve as a marker at birth that predicts risk of adiposity, informing the need for additional clinical monitoring or alternative nutritional recommendations to prevent exacerbated growth.

For my NORC pilot award I propose to determine whether intrauterine exposure to maternal concentrations of folate and choline through 27 weeks gestation influences offspring adiposity and is mediated by DNA methylation identified at birth by leveraging data obtained from the Healthy Start Study (R01 DK076648, PI: Dabelea) an ongoing a large, multi-ethnic, prebirth cohort that has collected DNA methylation at birth in ~600 infants and longitudinal adiposity measures at birth, 5 months, and 5 years of age in the offspring.  More specifically, in this population of mother-infant dyads in which maternal intake of these two 1-carbon nutrient precursors is outside of recommended intake ranges during pregnancy, I aim to 1) precisely elucidate the effect of excessive folate status and inadequate choline status, based on maternal serum concentrations, on infant and child adiposity outcomes, and 2) examine mediation by DNA methylation in offspring cord blood.  Our results will contribute to knowledge and may clarify rising concerns regarding “population wide excess folate status” especially in pregnant women due to dose exposure and the potential for long term adverse effects on offspring health. This investigation will also indicate whether such status has any potential compensatory effect on offspring anthropometric outcomes or DNA methylation in the context of low choline concentrations amongst the population of maternal-infant dyads studied.  Additionally, the NORC award will facilitate my career goals of obtaining a future career development grant and establishing independently funded research.

Dates of Funding: 2022-2024
I am a Post-doctoral Fellow in the Department of Pediatrics, Section of Nutrition at the University of Colorado – Anschutz Medical Center, supported by the Ruth L. Kirschstein National Research Service Award T32 Research Fellowship in Nutrition at the University of Colorado – Anschutz Medical Campus (CU – Anschutz). My research interest is in understanding the interactions of nutrition, maternal intrauterine exposures, and epigenetics on obesity risk in childhood. My long-term career goal is to establish myself as an independent physician scientist critically assessing the most optimal nutritional strategies for children at high risk of obesity and associated co-morbidities in the context of their interaction with genetic predisposition, susceptibility conferred via intrauterine exposures, and their effects on infant and child growth.  My interests lie in understanding the how the totality of these exposures and potential predictors can be moderated by evidence based nutritional interventions established earlier and sustained throughout the life course. 

Differences in childhood obesity risk may appear in infancy, suggesting that factors driving obesity begin operating very early in life. Neural, metabolic, and hormonal networks regulating energy balance are established in utero and are likely influenced by maternal exposures, including nutrition. Human studies have shown that such networks may be determined by epigenetic modifications, of which DNA methylation is the most well studied to date. Studies also indicate that maternal one carbon (1C) nutrient intake, such as that of folate and choline, peri-conceptionally and during pregnancy can influence both offspring adiposity and DNA methylation. Few studies, however, have aimed to evaluate the mediation of adiposity risk by DNA methylation in relation to its association with maternal 1C nutrient concentrations.  Differential DNA methylation, influenced by maternal 1C nutrient status, may serve as a marker at birth that predicts risk of adiposity, informing the need for additional clinical monitoring or alternative nutritional recommendations to prevent exacerbated growth.

For my NORC pilot award I propose to determine whether intrauterine exposure to maternal concentrations of folate and choline through 27 weeks gestation influences offspring adiposity and is mediated by DNA methylation identified at birth by leveraging data obtained from the Healthy Start Study (R01 DK076648, PI: Dabelea) an ongoing a large, multi-ethnic, prebirth cohort that has collected DNA methylation at birth in ~600 infants and longitudinal adiposity measures at birth, 5 months, and 5 years of age in the offspring.  More specifically, in this population of mother-infant dyads in which maternal intake of these two 1-carbon nutrient precursors is outside of recommended intake ranges during pregnancy, I aim to 1) precisely elucidate the effect of excessive folate status and inadequate choline status, based on maternal serum concentrations, on infant and child adiposity outcomes, and 2) examine mediation by DNA methylation in offspring cord blood.  Our results will contribute to knowledge and may clarify rising concerns regarding “population wide excess folate status” especially in pregnant women due to dose exposure and the potential for long term adverse effects on offspring health. This investigation will also indicate whether such status has any potential compensatory effect on offspring anthropometric outcomes or DNA methylation in the context of low choline concentrations amongst the population of maternal-infant dyads studied.  Additionally, the NORC award will facilitate my career goals of obtaining a future career development grant and establishing independently funded research.

Dates of Funding: 2022-2024
I am a Post-doctoral Fellow in the Department of Pediatrics, Section of Nutrition at the University of Colorado – Anschutz Medical Center, supported by the Ruth L. Kirschstein National Research Service Award T32 Research Fellowship in Nutrition at the University of Colorado – Anschutz Medical Campus (CU – Anschutz). My research interest is in understanding the interactions of nutrition, maternal intrauterine exposures, and epigenetics on obesity risk in childhood. My long-term career goal is to establish myself as an independent physician scientist critically assessing the most optimal nutritional strategies for children at high risk of obesity and associated co-morbidities in the context of their interaction with genetic predisposition, susceptibility conferred via intrauterine exposures, and their effects on infant and child growth.  My interests lie in understanding the how the totality of these exposures and potential predictors can be moderated by evidence based nutritional interventions established earlier and sustained throughout the life course. 

Differences in childhood obesity risk may appear in infancy, suggesting that factors driving obesity begin operating very early in life. Neural, metabolic, and hormonal networks regulating energy balance are established in utero and are likely influenced by maternal exposures, including nutrition. Human studies have shown that such networks may be determined by epigenetic modifications, of which DNA methylation is the most well studied to date. Studies also indicate that maternal one carbon (1C) nutrient intake, such as that of folate and choline, peri-conceptionally and during pregnancy can influence both offspring adiposity and DNA methylation. Few studies, however, have aimed to evaluate the mediation of adiposity risk by DNA methylation in relation to its association with maternal 1C nutrient concentrations.  Differential DNA methylation, influenced by maternal 1C nutrient status, may serve as a marker at birth that predicts risk of adiposity, informing the need for additional clinical monitoring or alternative nutritional recommendations to prevent exacerbated growth.

For my NORC pilot award I propose to determine whether intrauterine exposure to maternal concentrations of folate and choline through 27 weeks gestation influences offspring adiposity and is mediated by DNA methylation identified at birth by leveraging data obtained from the Healthy Start Study (R01 DK076648, PI: Dabelea) an ongoing a large, multi-ethnic, prebirth cohort that has collected DNA methylation at birth in ~600 infants and longitudinal adiposity measures at birth, 5 months, and 5 years of age in the offspring.  More specifically, in this population of mother-infant dyads in which maternal intake of these two 1-carbon nutrient precursors is outside of recommended intake ranges during pregnancy, I aim to 1) precisely elucidate the effect of excessive folate status and inadequate choline status, based on maternal serum concentrations, on infant and child adiposity outcomes, and 2) examine mediation by DNA methylation in offspring cord blood.  Our results will contribute to knowledge and may clarify rising concerns regarding “population wide excess folate status” especially in pregnant women due to dose exposure and the potential for long term adverse effects on offspring health. This investigation will also indicate whether such status has any potential compensatory effect on offspring anthropometric outcomes or DNA methylation in the context of low choline concentrations amongst the population of maternal-infant dyads studied.  Additionally, the NORC award will facilitate my career goals of obtaining a future career development grant and establishing independently funded research.

Dates of Funding: 2022-2024
I am a Post-doctoral Fellow in the Department of Pediatrics, Section of Nutrition at the University of Colorado – Anschutz Medical Center, supported by the Ruth L. Kirschstein National Research Service Award T32 Research Fellowship in Nutrition at the University of Colorado – Anschutz Medical Campus (CU – Anschutz). My research interest is in understanding the interactions of nutrition, maternal intrauterine exposures, and epigenetics on obesity risk in childhood. My long-term career goal is to establish myself as an independent physician scientist critically assessing the most optimal nutritional strategies for children at high risk of obesity and associated co-morbidities in the context of their interaction with genetic predisposition, susceptibility conferred via intrauterine exposures, and their effects on infant and child growth.  My interests lie in understanding the how the totality of these exposures and potential predictors can be moderated by evidence based nutritional interventions established earlier and sustained throughout the life course. 

Differences in childhood obesity risk may appear in infancy, suggesting that factors driving obesity begin operating very early in life. Neural, metabolic, and hormonal networks regulating energy balance are established in utero and are likely influenced by maternal exposures, including nutrition. Human studies have shown that such networks may be determined by epigenetic modifications, of which DNA methylation is the most well studied to date. Studies also indicate that maternal one carbon (1C) nutrient intake, such as that of folate and choline, peri-conceptionally and during pregnancy can influence both offspring adiposity and DNA methylation. Few studies, however, have aimed to evaluate the mediation of adiposity risk by DNA methylation in relation to its association with maternal 1C nutrient concentrations.  Differential DNA methylation, influenced by maternal 1C nutrient status, may serve as a marker at birth that predicts risk of adiposity, informing the need for additional clinical monitoring or alternative nutritional recommendations to prevent exacerbated growth.

For my NORC pilot award I propose to determine whether intrauterine exposure to maternal concentrations of folate and choline through 27 weeks gestation influences offspring adiposity and is mediated by DNA methylation identified at birth by leveraging data obtained from the Healthy Start Study (R01 DK076648, PI: Dabelea) an ongoing a large, multi-ethnic, prebirth cohort that has collected DNA methylation at birth in ~600 infants and longitudinal adiposity measures at birth, 5 months, and 5 years of age in the offspring.  More specifically, in this population of mother-infant dyads in which maternal intake of these two 1-carbon nutrient precursors is outside of recommended intake ranges during pregnancy, I aim to 1) precisely elucidate the effect of excessive folate status and inadequate choline status, based on maternal serum concentrations, on infant and child adiposity outcomes, and 2) examine mediation by DNA methylation in offspring cord blood.  Our results will contribute to knowledge and may clarify rising concerns regarding “population wide excess folate status” especially in pregnant women due to dose exposure and the potential for long term adverse effects on offspring health. This investigation will also indicate whether such status has any potential compensatory effect on offspring anthropometric outcomes or DNA methylation in the context of low choline concentrations amongst the population of maternal-infant dyads studied.  Additionally, the NORC award will facilitate my career goals of obtaining a future career development grant and establishing independently funded research.

Dates of Funding: 2022-2024
I am a Post-doctoral Fellow in the Department of Pediatrics, Section of Nutrition at the University of Colorado – Anschutz Medical Center, supported by the Ruth L. Kirschstein National Research Service Award T32 Research Fellowship in Nutrition at the University of Colorado – Anschutz Medical Campus (CU – Anschutz). My research interest is in understanding the interactions of nutrition, maternal intrauterine exposures, and epigenetics on obesity risk in childhood. My long-term career goal is to establish myself as an independent physician scientist critically assessing the most optimal nutritional strategies for children at high risk of obesity and associated co-morbidities in the context of their interaction with genetic predisposition, susceptibility conferred via intrauterine exposures, and their effects on infant and child growth.  My interests lie in understanding the how the totality of these exposures and potential predictors can be moderated by evidence based nutritional interventions established earlier and sustained throughout the life course. 

Differences in childhood obesity risk may appear in infancy, suggesting that factors driving obesity begin operating very early in life. Neural, metabolic, and hormonal networks regulating energy balance are established in utero and are likely influenced by maternal exposures, including nutrition. Human studies have shown that such networks may be determined by epigenetic modifications, of which DNA methylation is the most well studied to date. Studies also indicate that maternal one carbon (1C) nutrient intake, such as that of folate and choline, peri-conceptionally and during pregnancy can influence both offspring adiposity and DNA methylation. Few studies, however, have aimed to evaluate the mediation of adiposity risk by DNA methylation in relation to its association with maternal 1C nutrient concentrations.  Differential DNA methylation, influenced by maternal 1C nutrient status, may serve as a marker at birth that predicts risk of adiposity, informing the need for additional clinical monitoring or alternative nutritional recommendations to prevent exacerbated growth.

For my NORC pilot award I propose to determine whether intrauterine exposure to maternal concentrations of folate and choline through 27 weeks gestation influences offspring adiposity and is mediated by DNA methylation identified at birth by leveraging data obtained from the Healthy Start Study (R01 DK076648, PI: Dabelea) an ongoing a large, multi-ethnic, prebirth cohort that has collected DNA methylation at birth in ~600 infants and longitudinal adiposity measures at birth, 5 months, and 5 years of age in the offspring.  More specifically, in this population of mother-infant dyads in which maternal intake of these two 1-carbon nutrient precursors is outside of recommended intake ranges during pregnancy, I aim to 1) precisely elucidate the effect of excessive folate status and inadequate choline status, based on maternal serum concentrations, on infant and child adiposity outcomes, and 2) examine mediation by DNA methylation in offspring cord blood.  Our results will contribute to knowledge and may clarify rising concerns regarding “population wide excess folate status” especially in pregnant women due to dose exposure and the potential for long term adverse effects on offspring health. This investigation will also indicate whether such status has any potential compensatory effect on offspring anthropometric outcomes or DNA methylation in the context of low choline concentrations amongst the population of maternal-infant dyads studied.  Additionally, the NORC award will facilitate my career goals of obtaining a future career development grant and establishing independently funded research.

Dates of Funding: 2022-2024
I am a Post-doctoral Fellow in the Department of Pediatrics, Section of Nutrition at the University of Colorado – Anschutz Medical Center, supported by the Ruth L. Kirschstein National Research Service Award T32 Research Fellowship in Nutrition at the University of Colorado – Anschutz Medical Campus (CU – Anschutz). My research interest is in understanding the interactions of nutrition, maternal intrauterine exposures, and epigenetics on obesity risk in childhood. My long-term career goal is to establish myself as an independent physician scientist critically assessing the most optimal nutritional strategies for children at high risk of obesity and associated co-morbidities in the context of their interaction with genetic predisposition, susceptibility conferred via intrauterine exposures, and their effects on infant and child growth.  My interests lie in understanding the how the totality of these exposures and potential predictors can be moderated by evidence based nutritional interventions established earlier and sustained throughout the life course. 

Differences in childhood obesity risk may appear in infancy, suggesting that factors driving obesity begin operating very early in life. Neural, metabolic, and hormonal networks regulating energy balance are established in utero and are likely influenced by maternal exposures, including nutrition. Human studies have shown that such networks may be determined by epigenetic modifications, of which DNA methylation is the most well studied to date. Studies also indicate that maternal one carbon (1C) nutrient intake, such as that of folate and choline, peri-conceptionally and during pregnancy can influence both offspring adiposity and DNA methylation. Few studies, however, have aimed to evaluate the mediation of adiposity risk by DNA methylation in relation to its association with maternal 1C nutrient concentrations.  Differential DNA methylation, influenced by maternal 1C nutrient status, may serve as a marker at birth that predicts risk of adiposity, informing the need for additional clinical monitoring or alternative nutritional recommendations to prevent exacerbated growth.

For my NORC pilot award I propose to determine whether intrauterine exposure to maternal concentrations of folate and choline through 27 weeks gestation influences offspring adiposity and is mediated by DNA methylation identified at birth by leveraging data obtained from the Healthy Start Study (R01 DK076648, PI: Dabelea) an ongoing a large, multi-ethnic, prebirth cohort that has collected DNA methylation at birth in ~600 infants and longitudinal adiposity measures at birth, 5 months, and 5 years of age in the offspring.  More specifically, in this population of mother-infant dyads in which maternal intake of these two 1-carbon nutrient precursors is outside of recommended intake ranges during pregnancy, I aim to 1) precisely elucidate the effect of excessive folate status and inadequate choline status, based on maternal serum concentrations, on infant and child adiposity outcomes, and 2) examine mediation by DNA methylation in offspring cord blood.  Our results will contribute to knowledge and may clarify rising concerns regarding “population wide excess folate status” especially in pregnant women due to dose exposure and the potential for long term adverse effects on offspring health. This investigation will also indicate whether such status has any potential compensatory effect on offspring anthropometric outcomes or DNA methylation in the context of low choline concentrations amongst the population of maternal-infant dyads studied.  Additionally, the NORC award will facilitate my career goals of obtaining a future career development grant and establishing independently funded research.

Dates of Funding: 2022-2024
I am a Post-doctoral Fellow in the Department of Pediatrics, Section of Nutrition at the University of Colorado – Anschutz Medical Center, supported by the Ruth L. Kirschstein National Research Service Award T32 Research Fellowship in Nutrition at the University of Colorado – Anschutz Medical Campus (CU – Anschutz). My research interest is in understanding the interactions of nutrition, maternal intrauterine exposures, and epigenetics on obesity risk in childhood. My long-term career goal is to establish myself as an independent physician scientist critically assessing the most optimal nutritional strategies for children at high risk of obesity and associated co-morbidities in the context of their interaction with genetic predisposition, susceptibility conferred via intrauterine exposures, and their effects on infant and child growth.  My interests lie in understanding the how the totality of these exposures and potential predictors can be moderated by evidence based nutritional interventions established earlier and sustained throughout the life course. 

Differences in childhood obesity risk may appear in infancy, suggesting that factors driving obesity begin operating very early in life. Neural, metabolic, and hormonal networks regulating energy balance are established in utero and are likely influenced by maternal exposures, including nutrition. Human studies have shown that such networks may be determined by epigenetic modifications, of which DNA methylation is the most well studied to date. Studies also indicate that maternal one carbon (1C) nutrient intake, such as that of folate and choline, peri-conceptionally and during pregnancy can influence both offspring adiposity and DNA methylation. Few studies, however, have aimed to evaluate the mediation of adiposity risk by DNA methylation in relation to its association with maternal 1C nutrient concentrations.  Differential DNA methylation, influenced by maternal 1C nutrient status, may serve as a marker at birth that predicts risk of adiposity, informing the need for additional clinical monitoring or alternative nutritional recommendations to prevent exacerbated growth.

For my NORC pilot award I propose to determine whether intrauterine exposure to maternal concentrations of folate and choline through 27 weeks gestation influences offspring adiposity and is mediated by DNA methylation identified at birth by leveraging data obtained from the Healthy Start Study (R01 DK076648, PI: Dabelea) an ongoing a large, multi-ethnic, prebirth cohort that has collected DNA methylation at birth in ~600 infants and longitudinal adiposity measures at birth, 5 months, and 5 years of age in the offspring.  More specifically, in this population of mother-infant dyads in which maternal intake of these two 1-carbon nutrient precursors is outside of recommended intake ranges during pregnancy, I aim to 1) precisely elucidate the effect of excessive folate status and inadequate choline status, based on maternal serum concentrations, on infant and child adiposity outcomes, and 2) examine mediation by DNA methylation in offspring cord blood.  Our results will contribute to knowledge and may clarify rising concerns regarding “population wide excess folate status” especially in pregnant women due to dose exposure and the potential for long term adverse effects on offspring health. This investigation will also indicate whether such status has any potential compensatory effect on offspring anthropometric outcomes or DNA methylation in the context of low choline concentrations amongst the population of maternal-infant dyads studied.  Additionally, the NORC award will facilitate my career goals of obtaining a future career development grant and establishing independently funded research.