Stress and pregnancy don't mix well. One of the concerns arising from this mix has been the risk of autism. Acknowledging this danger should not trigger a vicious cycle of stressing about stress. That counter-productive process can and needs to be counter-acted. Nonetheless, knowledge is essential for a safe pregnancy.
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 second consideration is being aware of the proportionality dilemma. There is no doubt valuable insight from pumping mice full of some toxin vastly out of proportion to its use by most humans. Predicting effects from actual human use, though, isn't likely one of them.
This consideration demands reflection when we see that the researchers in the studies considered here describe the stress that they imposed on the research mice as being mild. This is not a precisely measurable term and begs all sorts of questions that require precision. Consequently, application of such findings to the human context is fraught with methodological ambiguity. The knowledge gap left wide open by this terminology must not be filled with baseless assumptions fueled by our anxieties.
Keeping those qualifications close at hand, it is true that experimental research has demonstrated in mice the placenta can transmit biochemical effects of stress to the fetus. The key factor here is an enzyme called OGT. Research suggests the OGT is 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?
Whatever the appropriate description of stress level in the mice, though, it seems to correlate to significantly reduced OGT levels. These reduced OGT levels triggered changes in excess of 370 of the unborn 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.
This discovery points to an important difference between boy and girl fetuses. Males have a naturally lower level of OGT. Thus, stress in pregnancy that is sufficient to reduce OGT will likely have a greater impact on boys. This might explain the higher frequency of autism and schizophrenia documented among 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 second consideration is being aware of the proportionality dilemma. There is no doubt valuable insight from pumping mice full of some toxin vastly out of proportion to its use by most humans. Predicting effects from actual human use, though, isn't likely one of them.
This consideration demands reflection when we see that the researchers in the studies considered here describe the stress that they imposed on the research mice as being mild. This is not a precisely measurable term and begs all sorts of questions that require precision. Consequently, application of such findings to the human context is fraught with methodological ambiguity. The knowledge gap left wide open by this terminology must not be filled with baseless assumptions fueled by our anxieties.
Keeping those qualifications close at hand, it is true that experimental research has demonstrated in mice the placenta can transmit biochemical effects of stress to the fetus. The key factor here is an enzyme called OGT. Research suggests the OGT is 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?
Whatever the appropriate description of stress level in the mice, though, it seems to correlate to significantly reduced OGT levels. These reduced OGT levels triggered changes in excess of 370 of the unborn 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.
This discovery points to an important difference between boy and girl fetuses. Males have a naturally lower level of OGT. Thus, stress in pregnancy that is sufficient to reduce OGT will likely have a greater impact on boys. This might explain the higher frequency of autism and schizophrenia documented among 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 birth supporters 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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