Stress and disease

Is being female a predisposing factor?

Jill B. Becker, Lisa M Monteggia, Tara S. Perrot-Sinal, Russell D. Romeo, Jane R. Taylor, Rachel Yehuda, Tracy L. Bale

Research output: Contribution to journalArticle

117 Citations (Scopus)

Abstract

Because the reported heightened female predisposition in these diseases seems to present after puberty, determination of stress pathway maturation may shed light on whether differences in disease presentation, treatment, and risk are a function of gonadal hormone profiles and/or more inherent to genetic sex (Fig. 2). Unarguably, our work in understanding sex differences in these diseases has just scratched the surface. We have only begun exploring the possible involvement of exciting areas such as intrauterine environment, epigenetics, and proteomics in longterm disease risk. An even greater scarcity exists for information on how these regulatory mechanisms could be built into sex-specific outcomes. It is clear, to answer the question of whether "being female is a predisposing factor," we are in desperate need of novel animal models and paradigms (Kalueff et al., 2007), in which such comparisons can be carefully studied.

Original languageEnglish (US)
Pages (from-to)11851-11855
Number of pages5
JournalJournal of Neuroscience
Volume27
Issue number44
DOIs
StatePublished - Oct 31 2007

Fingerprint

Causality
Gonadal Hormones
Puberty
Epigenomics
Sex Characteristics
Proteomics
Animal Models

Keywords

  • Addiction
  • Animal models
  • Depression
  • HPA axis
  • Sex
  • Stress

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Becker, J. B., Monteggia, L. M., Perrot-Sinal, T. S., Romeo, R. D., Taylor, J. R., Yehuda, R., & Bale, T. L. (2007). Stress and disease: Is being female a predisposing factor? Journal of Neuroscience, 27(44), 11851-11855. https://doi.org/10.1523/JNEUROSCI.3565-07.2007

Stress and disease : Is being female a predisposing factor? / Becker, Jill B.; Monteggia, Lisa M; Perrot-Sinal, Tara S.; Romeo, Russell D.; Taylor, Jane R.; Yehuda, Rachel; Bale, Tracy L.

In: Journal of Neuroscience, Vol. 27, No. 44, 31.10.2007, p. 11851-11855.

Research output: Contribution to journalArticle

Becker, JB, Monteggia, LM, Perrot-Sinal, TS, Romeo, RD, Taylor, JR, Yehuda, R & Bale, TL 2007, 'Stress and disease: Is being female a predisposing factor?', Journal of Neuroscience, vol. 27, no. 44, pp. 11851-11855. https://doi.org/10.1523/JNEUROSCI.3565-07.2007
Becker JB, Monteggia LM, Perrot-Sinal TS, Romeo RD, Taylor JR, Yehuda R et al. Stress and disease: Is being female a predisposing factor? Journal of Neuroscience. 2007 Oct 31;27(44):11851-11855. https://doi.org/10.1523/JNEUROSCI.3565-07.2007
Becker, Jill B. ; Monteggia, Lisa M ; Perrot-Sinal, Tara S. ; Romeo, Russell D. ; Taylor, Jane R. ; Yehuda, Rachel ; Bale, Tracy L. / Stress and disease : Is being female a predisposing factor?. In: Journal of Neuroscience. 2007 ; Vol. 27, No. 44. pp. 11851-11855.
@article{f0ff7785c94d44a3b6f29be0b856e076,
title = "Stress and disease: Is being female a predisposing factor?",
abstract = "Because the reported heightened female predisposition in these diseases seems to present after puberty, determination of stress pathway maturation may shed light on whether differences in disease presentation, treatment, and risk are a function of gonadal hormone profiles and/or more inherent to genetic sex (Fig. 2). Unarguably, our work in understanding sex differences in these diseases has just scratched the surface. We have only begun exploring the possible involvement of exciting areas such as intrauterine environment, epigenetics, and proteomics in longterm disease risk. An even greater scarcity exists for information on how these regulatory mechanisms could be built into sex-specific outcomes. It is clear, to answer the question of whether {"}being female is a predisposing factor,{"} we are in desperate need of novel animal models and paradigms (Kalueff et al., 2007), in which such comparisons can be carefully studied.",
keywords = "Addiction, Animal models, Depression, HPA axis, Sex, Stress",
author = "Becker, {Jill B.} and Monteggia, {Lisa M} and Perrot-Sinal, {Tara S.} and Romeo, {Russell D.} and Taylor, {Jane R.} and Rachel Yehuda and Bale, {Tracy L.}",
year = "2007",
month = "10",
day = "31",
doi = "10.1523/JNEUROSCI.3565-07.2007",
language = "English (US)",
volume = "27",
pages = "11851--11855",
journal = "Journal of Neuroscience",
issn = "0270-6474",
publisher = "Society for Neuroscience",
number = "44",

}

TY - JOUR

T1 - Stress and disease

T2 - Is being female a predisposing factor?

AU - Becker, Jill B.

AU - Monteggia, Lisa M

AU - Perrot-Sinal, Tara S.

AU - Romeo, Russell D.

AU - Taylor, Jane R.

AU - Yehuda, Rachel

AU - Bale, Tracy L.

PY - 2007/10/31

Y1 - 2007/10/31

N2 - Because the reported heightened female predisposition in these diseases seems to present after puberty, determination of stress pathway maturation may shed light on whether differences in disease presentation, treatment, and risk are a function of gonadal hormone profiles and/or more inherent to genetic sex (Fig. 2). Unarguably, our work in understanding sex differences in these diseases has just scratched the surface. We have only begun exploring the possible involvement of exciting areas such as intrauterine environment, epigenetics, and proteomics in longterm disease risk. An even greater scarcity exists for information on how these regulatory mechanisms could be built into sex-specific outcomes. It is clear, to answer the question of whether "being female is a predisposing factor," we are in desperate need of novel animal models and paradigms (Kalueff et al., 2007), in which such comparisons can be carefully studied.

AB - Because the reported heightened female predisposition in these diseases seems to present after puberty, determination of stress pathway maturation may shed light on whether differences in disease presentation, treatment, and risk are a function of gonadal hormone profiles and/or more inherent to genetic sex (Fig. 2). Unarguably, our work in understanding sex differences in these diseases has just scratched the surface. We have only begun exploring the possible involvement of exciting areas such as intrauterine environment, epigenetics, and proteomics in longterm disease risk. An even greater scarcity exists for information on how these regulatory mechanisms could be built into sex-specific outcomes. It is clear, to answer the question of whether "being female is a predisposing factor," we are in desperate need of novel animal models and paradigms (Kalueff et al., 2007), in which such comparisons can be carefully studied.

KW - Addiction

KW - Animal models

KW - Depression

KW - HPA axis

KW - Sex

KW - Stress

UR - http://www.scopus.com/inward/record.url?scp=35948980464&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=35948980464&partnerID=8YFLogxK

U2 - 10.1523/JNEUROSCI.3565-07.2007

DO - 10.1523/JNEUROSCI.3565-07.2007

M3 - Article

VL - 27

SP - 11851

EP - 11855

JO - Journal of Neuroscience

JF - Journal of Neuroscience

SN - 0270-6474

IS - 44

ER -