Pablo A. Nepomnaschy

Dr. Pablo A. Nepomnaschy

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Research Focus & Metrics

Academic Career Length

23Years (2004-Present)

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

Representative Publications

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22 February 2006 in Proceedings of the National Academy of Sciences
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Journal Article
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PNPablo A. Nepomnaschy
Pablo A. Nepomnaschy
KWKathleen B. Welch
Kathleen B. Welch
DMDaniel S. McConnell
Daniel S. McConnell
BLBobbi S. Low
Bobbi S. Low
BSBeverly I. Strassmann
Beverly I. Strassmann
BEBarry G. England
Barry G. England
Maternal stress is commonly cited as an important risk factor for spontaneous abortion. For humans, however, there is little physiological evidence linking miscarriage to stress. This lack of evidence may be attributable to a paucity of research on maternal stress during the earliest gestational stages. Most human studies have focused on “clinical” pregnancy (>6 weeks after the last menstrual period). The majority of miscarriages, however, occur earlier, within the first 3 weeks after conception (≈5 weeks after the last menstrual period). Studies focused on clinical pregnancy thus miss the most critical period for pregnancy continuance. We examined the association between miscarriage and levels of maternal urinary cortisol during the first 3 weeks after conception. Pregnancies characterized by increased maternal cortisol during this period (within participant analyses) were more likely to result in spontaneous abortion ( P < 0.05). This evidence links increased levels in this stress marker with a higher risk of early pregnancy loss in humans.

1 June 2011 in Neuroscience & Biobehavioral Reviews
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MFMark V. Flinn
Mark V. Flinn
PNPablo A. Nepomnaschy
Pablo A. Nepomnaschy
MMMichael P. Muehlenbein
Michael P. Muehlenbein
DPDavide Ponzi
Davide Ponzi

13 August 2004 in American Journal of Human Biology
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Journal Article
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PNPablo A. Nepomnaschy
Pablo A. Nepomnaschy
KWKathy Welch
Kathy Welch
DMDan McConnell
Dan McConnell
BSBeverly I. Strassmann
Beverly I. Strassmann
BEBarry G. England
Barry G. England

1 August 2009 in Environmental Research
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Journal Article
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PNPablo A. Nepomnaschy
Pablo A. Nepomnaschy
DBDonna Baird
Donna Baird
CWClarice R. Weinberg
Clarice R. Weinberg
JHJane A. Hoppin
Jane A. Hoppin
MLMatthew Longnecker
Matthew Longnecker
AWAllen J. Wilcox
Allen J. Wilcox

1 October 2007 in Annals of the New York Academy of Sciences
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Journal Article
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PNPablo A. Nepomnaschy
Pablo A. Nepomnaschy
ESEyal Sheiner
Eyal Sheiner
GMGeorge Mastorakos
George Mastorakos
PAPetra C. Arck
Petra C. Arck

5 January 2016 in PLOS ONE
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Journal Article
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CBCindy K. Barha
Cindy K. Barha
CHCourtney W. Hanna
Courtney W. Hanna
KSKatrina G. Salvante
Katrina G. Salvante
SWSamantha L. Wilson
Samantha L. Wilson
WRWendy Robinson
Wendy Robinson
PNPablo A. Nepomnaschy
Pablo A. Nepomnaschy
Life history theory (LHT) predicts a trade-off between reproductive effort and the pace of biological aging. Energy invested in reproduction is not available for tissue maintenance, thus having more offspring is expected to lead to accelerated senescence. Studies conducted in a variety of non-human species are consistent with this LHT prediction. Here we investigate the relationship between the number of surviving children born to a woman and telomere length (TL, a marker of cellular aging) over 13 years in a group of 75 Kaqchikel Mayan women. Contrary to LHT’s prediction, women who had fewer children exhibited shorter TLs than those who had more children (p = 0.045) after controlling for TL at the onset of the 13-year study period. An “ultimate” explanation for this apparently protective effect of having more children may lay with human’s cooperative-breeding strategy. In a number of socio-economic and cultural contexts, having more chilren appears to be linked to an increase in social support for mothers (e.g., allomaternal care). Higher social support, has been argued to reduce the costs of further reproduction. Lower reproductive costs may make more metabolic energy available for tissue maintenance, resulting in a slower pace of cellular aging. At a “proximate” level, mechanisms involved may include the actions of the gonadal steroid estradiol, which increases dramatically during pregnancy. Estradiol is known to protect TL from the effects of oxidative stress as well as increase telomerase activity, an enzyme that maintains TL. Future research should explore the potential role of social support as well as that of estradiol and other potential biological pathways in the trade-offs between reproductive effort and the pace of cellular aging within and among human as well as in non-human populations.