When considering the relationship of stress and pregnancy an issue that needs to be addressed is concerns about autism. I've insisted elsewhere on how destructive can be the vicious cycle of stressing about stress. This doesn't change the fact though that you still need to be informed. You just need to keep the information in context.
Pregnant woman and their partners are better served by awareness of recent research drawing connections between pregnancy stress and autism risks. It is essential though to not overreact and maintain a broader perspective on the evidence.
The evidence thus far is derived from mice studies. Certainly mice-based research has provided valuable medical advances and scientific insights into human disease patterns and processes. It would be a major logical fallacy though to simply assume any evidence from mice studies automatically and immediately applies to humans. That is a separate question, which has to be evaluated on its intrinsic merits.
The always delicate question of relevant proportionality is a case in point. For example, the common enough practice of pumping mice with levels of a toxin which have no relation to disproportional usage commonly practiced by humans is indeed scientifically relevant and valuable. It is not, though, in any way a sound basis from which to predict effects from the more modest human use patterns. Such extrapolation would not be methodologically sound.
This is important to remember when we observe that the researchers characterize the stress imposed on the mice as mild. This term though reveals nothing precise about the stress level of the mice. Nor does it reveal whether such findings do (or don't) translate to human experience. The resulting knowledge gap should not be filled with baseless assumptions fueled by our worst fears.
With those caveats in mind, research is showing that an expectant mother's placenta can transmit biochemical effects of stress to her unborn child. An enzyme called OGT appears to be inhibited in the placenta of mice subjected to what researchers call mild stress.
It is valuable to observe that this mouse stress was generated through exposure to both unfamiliar noises and to the scent of foxes. This author remains unclear as to why - since we know that scent reaction can be wired into the evolved psychology through natural selection - the stress caused by exposure to threat of a natural predator should be considered mild.
In any event, despite this serious flaw in the presentation of the research findings, it does appear clear that at some level of stress, mice do experience significantly reduced OGT levels. These reductions trigger alternations of over 370 of the mice's brain genes.
Furthermore, the specific neurons altered include those that are known to be important to developmental brain activities in the fetus. Among these activities are regulation of energy use, protein development and nerve cell connections. So, at least at some level of stress, it seems likely that OGT-driven brain developmental benefits are hurt by diminishing of the enzyme's levels.
Some corroborating evidence is also provided by comparing the expected differential results for male and female fetuses. Male fetuses have a naturally lower OGT level. So, it would be expected, whatever the level of stress sufficient to trigger reduced OGT, the impact upon male fetuses would be expected to be greater than that for girls: the deprivation level would be triggered earlier in males and tend to have worse consequences. This conjecture seems to be confirmed by the higher autism and schizophrenia rates recorded for males.
To repeat, this is valuable knowledge that expecting mothers and their partners should understand. As with all information, though, the correct response is not increased stress! Rather it is yet further reason to be proactive in reducing pregnancy stress. See our suggestions for solutions that work .
Pregnant woman and their partners are better served by awareness of recent research drawing connections between pregnancy stress and autism risks. It is essential though to not overreact and maintain a broader perspective on the evidence.
The evidence thus far is derived from mice studies. Certainly mice-based research has provided valuable medical advances and scientific insights into human disease patterns and processes. It would be a major logical fallacy though to simply assume any evidence from mice studies automatically and immediately applies to humans. That is a separate question, which has to be evaluated on its intrinsic merits.
The always delicate question of relevant proportionality is a case in point. For example, the common enough practice of pumping mice with levels of a toxin which have no relation to disproportional usage commonly practiced by humans is indeed scientifically relevant and valuable. It is not, though, in any way a sound basis from which to predict effects from the more modest human use patterns. Such extrapolation would not be methodologically sound.
This is important to remember when we observe that the researchers characterize the stress imposed on the mice as mild. This term though reveals nothing precise about the stress level of the mice. Nor does it reveal whether such findings do (or don't) translate to human experience. The resulting knowledge gap should not be filled with baseless assumptions fueled by our worst fears.
With those caveats in mind, research is showing that an expectant mother's placenta can transmit biochemical effects of stress to her unborn child. An enzyme called OGT appears to be inhibited in the placenta of mice subjected to what researchers call mild stress.
It is valuable to observe that this mouse stress was generated through exposure to both unfamiliar noises and to the scent of foxes. This author remains unclear as to why - since we know that scent reaction can be wired into the evolved psychology through natural selection - the stress caused by exposure to threat of a natural predator should be considered mild.
In any event, despite this serious flaw in the presentation of the research findings, it does appear clear that at some level of stress, mice do experience significantly reduced OGT levels. These reductions trigger alternations of over 370 of the mice's brain genes.
Furthermore, the specific neurons altered include those that are known to be important to developmental brain activities in the fetus. Among these activities are regulation of energy use, protein development and nerve cell connections. So, at least at some level of stress, it seems likely that OGT-driven brain developmental benefits are hurt by diminishing of the enzyme's levels.
Some corroborating evidence is also provided by comparing the expected differential results for male and female fetuses. Male fetuses have a naturally lower OGT level. So, it would be expected, whatever the level of stress sufficient to trigger reduced OGT, the impact upon male fetuses would be expected to be greater than that for girls: the deprivation level would be triggered earlier in males and tend to have worse consequences. This conjecture seems to be confirmed by the higher autism and schizophrenia rates recorded for males.
To repeat, this is valuable knowledge that expecting mothers and their partners should understand. As with all information, though, the correct response is not increased stress! Rather it is yet further reason to be proactive in reducing pregnancy stress. See our suggestions for solutions that work .
About the Author:
Expecting moms and their partners who want to keep up on all the relevant news need to follow the Stress and Pregnancy site. Also, for more great information about healthy life-choice, check out the info at our sister project, the Getting Rid of a Headache Without Medicine blog.
