hope
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Here is a study which I just recently read and thought very interesting. The content may not be news to everyone but the study itself is new and I thought perhaps others might like to give it a read.
We have known for some time how stress and diet etc. on the part of a potential mother may affect the unborn baby and even the future development of the child.[think also Maciamo`s recent post reg. pre-natal nicotine exposure.]
But now, according to a study with mice, done at the University of Pennsylvania, it seems stress on the part of the father may cause a change to his sperm This can in turn take a toll on the stress response of his offspring.
In the study, the male mice were subjected to chronic stress, including being exposed to the scent of predators, noise and new environments. This stress was shown to have an epigenetic effect to their sperm. The offspring of these mice had blunted stress responses with a change to the normal levels of corticosterone, the mouse equivalent of the human stress hormone, cortisol.
If the response to stress is not working normally, the research notes the potential for psychiatric disorders.
It would seem for anyone hoping to soon have a child, a low stress level is just as important for the father as the mother going by this.
So here is the original abstract from The Journal of Neuroscience..published this April.
Abstract
Neuropsychiatric disease frequently presents with an underlying hyporeactivity or hyperreactivity of the HPA stress axis, suggesting an exceptional vulnerability of this circuitry to external perturbations. Parental lifetime exposures to environmental challenges are associated with increased offspring neuropsychiatric disease risk, and likely contribute to stress dysregulation. While maternal influences have been extensively examined, much less is known regarding the specific role of paternal factors. To investigate the potential mechanisms by which paternal stress may contribute to offspring hypothalamic–pituitary–adrenal (HPA) axis dysregulation, we exposed mice to 6 weeks of chronic stress before breeding. As epidemiological studies support variation in paternal germ cell susceptibility to reprogramming across the lifespan, male stress exposure occurred either throughout puberty or in adulthood. Remarkably, offspring of sires from both paternal stress groups displayed significantly reduced HPA stress axis responsivity. Gene set enrichment analyses in offspring stress regulating brain regions, the paraventricular nucleus (PVN) and the bed nucleus of stria terminalis, revealed global pattern changes in transcription suggestive of epigenetic reprogramming and consistent with altered offspring stress responsivity, including increased expression of glucocorticoid-responsive genes in the PVN. In examining potential epigenetic mechanisms of germ cell transmission, we found robust changes in sperm microRNA (miR) content, where nine specific miRs were significantly increased in both paternal stress groups. Overall, these results demonstrate that paternal experience across the lifespan can induce germ cell epigenetic reprogramming and impact offspring HPA stress axis regulation, and may therefore offer novel insight into factors influencing neuropsychiatric disease risk.
We have known for some time how stress and diet etc. on the part of a potential mother may affect the unborn baby and even the future development of the child.[think also Maciamo`s recent post reg. pre-natal nicotine exposure.]
But now, according to a study with mice, done at the University of Pennsylvania, it seems stress on the part of the father may cause a change to his sperm This can in turn take a toll on the stress response of his offspring.
In the study, the male mice were subjected to chronic stress, including being exposed to the scent of predators, noise and new environments. This stress was shown to have an epigenetic effect to their sperm. The offspring of these mice had blunted stress responses with a change to the normal levels of corticosterone, the mouse equivalent of the human stress hormone, cortisol.
If the response to stress is not working normally, the research notes the potential for psychiatric disorders.
It would seem for anyone hoping to soon have a child, a low stress level is just as important for the father as the mother going by this.
So here is the original abstract from The Journal of Neuroscience..published this April.
Abstract
Neuropsychiatric disease frequently presents with an underlying hyporeactivity or hyperreactivity of the HPA stress axis, suggesting an exceptional vulnerability of this circuitry to external perturbations. Parental lifetime exposures to environmental challenges are associated with increased offspring neuropsychiatric disease risk, and likely contribute to stress dysregulation. While maternal influences have been extensively examined, much less is known regarding the specific role of paternal factors. To investigate the potential mechanisms by which paternal stress may contribute to offspring hypothalamic–pituitary–adrenal (HPA) axis dysregulation, we exposed mice to 6 weeks of chronic stress before breeding. As epidemiological studies support variation in paternal germ cell susceptibility to reprogramming across the lifespan, male stress exposure occurred either throughout puberty or in adulthood. Remarkably, offspring of sires from both paternal stress groups displayed significantly reduced HPA stress axis responsivity. Gene set enrichment analyses in offspring stress regulating brain regions, the paraventricular nucleus (PVN) and the bed nucleus of stria terminalis, revealed global pattern changes in transcription suggestive of epigenetic reprogramming and consistent with altered offspring stress responsivity, including increased expression of glucocorticoid-responsive genes in the PVN. In examining potential epigenetic mechanisms of germ cell transmission, we found robust changes in sperm microRNA (miR) content, where nine specific miRs were significantly increased in both paternal stress groups. Overall, these results demonstrate that paternal experience across the lifespan can induce germ cell epigenetic reprogramming and impact offspring HPA stress axis regulation, and may therefore offer novel insight into factors influencing neuropsychiatric disease risk.
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