Prenatal stress effects on offspring brain and behavior: Mediators, alterations and dysregulated epigenetic mechanisms

Haq, Shams Ul; Bhat, Unis Ahmad; Kumar, Arvind

doi:10.1007/s12038-021-00153-7

Cited by 22 publications

(13 citation statements)

References 176 publications

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“…Further, our findings in combination with prior evidence in the TRAILS sample suggests that both genetic (i.e., PRS smoking ) and “environmental catalysts” (in this case prenatal risk and less warm parenting) may operate partially by the blunting of the stress response [21]. There is accumulating evidence that prenatal stress can operate through multiple prenatal biological mechanisms (i.e., mediated by changes in cortisol, serotonin, cytokine, and microbiota in pregnant mothers) that are linked to alteration of several offspring neural phenotypes (e.g., neural circuit formation and pruning processes, brain structural connectivity, and/or epigenetic changes in neural gene expression) that can affect offspring cortisol reactivity [16, 34]. The resulting dysregulation of the stress response system then also may exacerbate these earlier-life influences on substance use.…”

Section: Discussionmentioning

confidence: 99%

Interactions between Genetic, Prenatal, Cortisol, and Parenting Influences on Adolescent Substance Use and Frequency: A TRAILS Study

et al. 2021

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Introduction: Dynamic relations between genetic, hormone, and pre- and postnatal environments are theorized as critically important for adolescent substance use but are rarely tested in multifactorial models. This study assessed the impact of interactions of genetic risk and cortisol reactivity with prenatal and parenting influences on both any and frequency of adolescent substance use. Methods: Data are from the TRacking Adolescents’ Individual Lives Survey (TRAILS), a prospective longitudinal, multi-rater study of 2,230 Dutch adolescents. Genetic risk was assessed via 3 substance-specific polygenic scores. Mothers retrospectively reported prenatal risk when adolescents were 11 years old. Adolescents rated their parents’ warmth and hostility at age 11. Salivary cortisol reactivity was measured in response to a social stress task at age 16. Adolescents’ self-reported cigarette, alcohol, and cannabis use frequency at age 16. Results: A multivariate hurdle regression model showed that polygenic risk for smoking, alcohol, and cannabis predicted any use of each substance, respectively, but predicted more frequent use only for smoking. Blunted cortisol reactivity predicted any use and more frequent use for all 3 outcomes. There were 2 interactions: blunted cortisol reactivity exacerbated the association of polygenic risk with any smoking and the association of prenatal risk with any alcohol use. Conclusion: Polygenic risk seems of importance for early use but less so for frequency of use, whereas blunted cortisol reactivity was correlated with both. Blunted cortisol reactivity may also catalyze early risks for substance use, though to a limited degree. Gene-environment interactions play no role in the context of this multifactorial model.

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Section: Discussionmentioning

confidence: 99%

Interactions between Genetic, Prenatal, Cortisol, and Parenting Influences on Adolescent Substance Use and Frequency: A TRAILS Study

et al. 2021

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“…Maternal stress during pregnancy seriously disturbs and alters epigenetic markers that can repress or facilitate the expression of associated genes, especially DNA methylation, one of the most widely studied mechanisms associated with long‐term effects on the stress‐exposure phenotype during pregnancy (Cao‐Lei et al, 2020). Evidence has increasingly demonstrated that prenatal stress exposure not only influences many relevant genes' expression related to the regulation of HPA axis function, such as stress‐related genes including NR3C1 (GR gene) and CRH (corticotrophin‐releasing hormone gene; Kertes et al, 2016; Mulligan et al, 2012) but also interferes with the expression of genes related to the placenta and brain tissues, with pivotal genes such as the 11β‐HSD‐2 gene and the brain‐derived neurotrophic factor gene (Haq et al, 2021). Epigenetic marks are mitotically stable and can, therefore, be maintained across generations (Skinner et al, 2010).…”

Section: Programming Effects Of Pmsmentioning

confidence: 99%

Development programming: Stress during gestation alters offspring development in sheep

Wei,

Gao,

Liu

et al. 2023

Reprod Domestic Animals

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Inappropriate management practices of domestic animals during pregnancy can be potential stressors, resulting in complex behavioural, physiological and neurological consequences in the developing offspring. Some of these consequences can last into adulthood or propagate to subsequent generations. We systematically summarized the results of different experimental patterns using artificially increased maternal glucocorticoid levels or prenatal maternal physiological stress paradigms, mediators between prenatal maternal stress (PMS) and programming effects in the offspring and the effects of PMS on offspring phenotypes in sheep. PMS can impair birthweight, regulate the development of the hypothalamic–pituitary–adrenal axis, modify behavioural patterns and cognitive abilities and alter gene expression and brain morphology in offspring. Further research should focus on the effects of programming on gene expression, immune function, gut microbiome, sex‐specific effects and maternal behaviour of offspring, especially comparative studies of gestational periods when PMS is applied, continual studies of programming effects on offspring and treatment strategies that effectively reverse the detrimental programming effects of prenatal stress.

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“…Prenatal exposure to ecological or social stressors (whether competition or social isolation) experienced by parents while offspring are in the womb or in the egg, may directly affect offspring neuroendocrine function (Sheriff et al, 2010;Love et al, 2013). For instance, mediations may occur via alterations of the expression/transcription of specific genes/proteins related to the programming/functioning of the stress axis (Marasco et al, 2016;D'Agostino et al, 2019;Mueller et al, 2021;Haq et al, 2021). Yet, the extent to which such effects are adaptive or not in ecological environments is unclear, and still under intense scrutiny (Sheriff and Love, 2013;Sheriff et al, 2017;Sopinka et al, 2017;Yin et al, 2019;Sánchez-Tójar et al, 2020;Zhang et al, 2020).…”

Section: Where Next?mentioning

confidence: 99%

Effects of the social environment on vertebrate fitness and health in nature: Moving beyond the stress axis

Lemonnier

Bize

Boonstra

et al. 2022

Hormones and Behavior

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Prenatal stress effects on offspring brain and behavior: Mediators, alterations and dysregulated epigenetic mechanisms

Cited by 22 publications

References 176 publications

Interactions between Genetic, Prenatal, Cortisol, and Parenting Influences on Adolescent Substance Use and Frequency: A TRAILS Study

Interactions between Genetic, Prenatal, Cortisol, and Parenting Influences on Adolescent Substance Use and Frequency: A TRAILS Study

Development programming: Stress during gestation alters offspring development in sheep

Effects of the social environment on vertebrate fitness and health in nature: Moving beyond the stress axis

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