The Autism Risk With Stress And Pregnancy
One consideration for thinking about the relation between stress and pregnancy is the matter of stress in pregnancy and autism. As we've emphasized elsewhere, stressing about stress is a counter-productive cycle that needs to be avoided. However, knowledge is valuable.
Expecting mothers - and their partners - need to know that there is increasing evidence that stress can be harmful to their unborn children, including increasing the possibility of autism. Before launching into the science, though, a couple qualifications are valuable.
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.
Bearing in mind such qualifications, we can observe the significance of research findings to the effect that the placenta of pregnant mice transmits biochemical effects of stress to the fetus. The essential element involved appears to be an enzyme called OGT. The relevant research indicates that OGT is what's inhibited in the placenta of mice who are subjected to what researchers describe as mild stress.
As suggested above, it is here that we need to be cautious. This mouse stress was generated by means of exposing them to both unfamiliar noises and to the scent of foxes. It is though well known that scent reaction can be wired into the evolved neural structure through natural selection. How then is it valid to characterize exposure to existential threat of a natural predator as a mild stress?
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.
These changed neurons are critical to neurological development, including regulation of energy use, protein development and nerve cell connections. It appears likely then that OGT helps protect the brain in pregnancy.
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.
As noted at the start, this kind of information is valuable for expecting mothers and their partners. It should though be empowering, not a source of increased stress. The basic rule remains that it is your job to take proactive measures reducing pregnancy stress. See our suggestions for solutions that work .
Expecting mothers - and their partners - need to know that there is increasing evidence that stress can be harmful to their unborn children, including increasing the possibility of autism. Before launching into the science, though, a couple qualifications are valuable.
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.
Bearing in mind such qualifications, we can observe the significance of research findings to the effect that the placenta of pregnant mice transmits biochemical effects of stress to the fetus. The essential element involved appears to be an enzyme called OGT. The relevant research indicates that OGT is what's inhibited in the placenta of mice who are subjected to what researchers describe as mild stress.
As suggested above, it is here that we need to be cautious. This mouse stress was generated by means of exposing them to both unfamiliar noises and to the scent of foxes. It is though well known that scent reaction can be wired into the evolved neural structure through natural selection. How then is it valid to characterize exposure to existential threat of a natural predator as a mild stress?
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.
These changed neurons are critical to neurological development, including regulation of energy use, protein development and nerve cell connections. It appears likely then that OGT helps protect the brain in pregnancy.
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.
As noted at the start, this kind of information is valuable for expecting mothers and their partners. It should though be empowering, not a source of increased stress. The basic rule remains that it is your job to take proactive measures 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.
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