The DOI matches its Crossref record; 61 of the 64 references it cites were found in a registry or an index.
Maternal smoking during pregnancy and infant stress response: Test of a prenatal programming hypothesis
Open accessAbstract
Background Maternal smoking during pregnancy (MSDP) is associated with early and long-term neurobehavioral deficits; however mechanisms remain unknown. We tested the hypothesis that MSDP programs the hypothalamic pituitary adrenocortical (HPA) axis of the offspring leading to adverse outcomes. In an intensive, prospective study, we investigated associations between MSDP and infant cortisol stress response and explored whether alterations in cortisol response were mediated by epigenetic modulation of the placental glucocorticoid receptor gene (NR3C1).Methods Participants were 100 healthy mother-infant pairs (53% MSDP-exposed; 42% female) from a low income, racially/ethnically diverse sample (55% minorities). MSDP was assessed by timeline followback interview verified by saliva and meconium cotinine. Infant cortisol responses to a neurobehavioral exam were assessed seven times over the first postnatal month. Methylation of placental NR3C1 promoter exon 1F was assessed using bisulfite pyrosequencing in a subsample (n=45).Results MSDP-exposed infants showed significantly and persistently attenuated basal and reactive cortisol levels over the first postnatal month vs. unexposed infants. Exploratory analyses revealed that MSDP was associated with altered methylation of the placental NR3C1 promoter; degree of methylation of the placental NR3C1 was associated with infant basal and reactive cortisol over the first postnatal month and mediated effects of MSDP on infant basal cortisol.Conclusions Results provide initial support for our hypothesis that MSDP programs offspring HPA (dys)regulation. Epigenetic regulation of placental GR may serve as a novel underlying mechanism. Results may have implications for delineating pathways to adverse outcomes from MSDP.
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“infants aged 1-7 months showed altered cortisol response to stress.”
From Developmental toxicity of nicotine: A transdisciplinary synthesis and implications for emerging tobacco products (2017) · cites this paper as [135]
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Palma-Gudiel, H., Córdova-Palomera, A., Leza, J. C., & Fañanás, L. (2015) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2015.05.016 · Cited by 347
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Maternal Factors that Induce Epigenetic Changes Contribute to Neurological Disorders in Offspring
Banik, A., Kandilya, D., Ramya, S., Stünkel, W., Chong, Y. S., & Dheen, S. T. (2017) · Genes · doi:10.3390/genes8060150 · Cited by 163
Metadata
- Authors
- Stroud, L. R., Papandonatos, G. D., Rodriguez, D., McCallum, M., Salisbury, A. L., Phipps, M. G., Lester, B., Huestis, M. A., Niaura, R., Padbury, J. F., & Marsit, C. J.
- Affiliations
- Brown University (US)
- La Salle University (US)
- Emory University (US)
- National Institutes of Health (US)
- Truth Initiative (US)
- Dartmouth College (US)
- Corresponding author
- Stroud, Laura R.
- ORCID
- Venue
- Psychoneuroendocrinology
- Publisher
- Elsevier BV
- Published
- 2014-10
- Volume
- 48
- Pages
- 29-40
- ISSN
- 0306-4530 (ISSN-L)
- PMC
- PMC4136384
- OpenAlex
- W2021299571
- Cited by
- 104
- References
- 64
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 5 · 2023: 4 · 2022: 8 · 2021: 12 · 2020: 11 · 2019: 6 · 2018: 15 · 2017: 7 · 2016: 16 · 2015: 8 · 2014: 3
- FWCI
- 10.65
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Psychoneuroendocrinology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Drug Abuse (R01DA019558, R01DA031188)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- smoking during pregnancy, infant cortisol, hypothalamic-pituitary-adrenal axis, prenatal programming, glucocorticoid receptor, NR3C1, DNA methylation, placenta, epigenetics, stress response, neurobehavioral outcomes, cotinine
- MeSH terms
- Adolescent, Adult, Female, Humans, Hydrocortisone, Infant, Newborn, Placenta, Pregnancy, Pregnancy Complications, Prenatal Exposure Delayed Effects, Receptors, Glucocorticoid, Smoking, Stress, Physiological, Case-Control Studies, DNA Methylation, Epigenesis, Genetic, Embryonic Development, Young Adult
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