We have earlier discussed factors that our research has indicated may have contributed to the increased incidence of Autistic Spectrum Disorders. Whatever factors are contributing to the growing incidence must have three qualities:

1) They must be increasing in human environments.
2) They must be widely distributed on the planet.
3) They must be (collectively) powerful in their impacts.

One striking aspects of the described increase in autism incidence is the continued strong co-inheritance of autism by identical twins. Environmental factors that increase the level of pathology to convert children who would not earlier be identified as autistic to kids who now meet the autism diagnostic criteria must be very reliably shared (at least almost always, by both twins) in their local environment.

I have earlier argued that the probable basis of autism is the inheritance of genetic faults potentially exacerbated by environmental factors that add to processing “noise” in the developing brain. Several hundred genetic faults affecting the maturation of inhibitory or excitatory processes in the brain, or affecting processes crucial to the brain’s experience-driven maturation could be expected to contribute additively to “brain noise” genesis.

As noted earlier, we have studied three environmental factors that meet the above three criteria:

1) acoustic, visual and other environmental “noise”

2) chemical toxins, with a non-coplanar PCB studied as a ‘placeholder’ for PCB and related PBDEs, which are still collectively increasing in quantity, in the environment (the literature also documents a variety of other chemical toxin candidates)

3) repeated ultrasound procedures

I would like to add (discuss) two more possible factors to this list.

4) SSRIs (selective serotonin receptor uptake inhibitors) = anti-depressants, commonly prescribed to pregnant mothers and/or nursing (as well as other commonly-prescribed psychoactive drugs); and

5) perinatal anoxia

The discussion of SSRIs is complicated, and because we (led by a collaborating scientist from the University of Mississippi, Dr. Rick Lin) are preparing a research report on this subject, I am going to hold it back when I can discuss it in more detail in a later blog. One important consideration: These drugs are used to help mothers in very important ways that contribute POSITIVELY to stable pregnancies and to successful infant nursing and rearing. Any potentially negative impacts that they may have on their infants must be weighed against these important counter-balancing positive factors.

Which brings us to perinatal anoxia. We have published compelling evidence that peri-natal anoxia meets all of the other criteria for adding to “noisy” brain processing. It can have strong, selective impacts on cortical inhibitory processes, and degrades the ability of the cortex to develop normally-selective characteristics of response (see Strata, Merzenich et al, PNAS, 2005). At the same time, we had dismissed perinatal anoxia as a likely factor contributing to autism’s apparent rise because we could not see how ITS incidence could be growing over the past several decades.

However, it has recently been argued that the especially high susceptibility of the highly metabolically active auditory brainstem to brief periods of anoxia that we and others have documented comes into play in the few to many tens of seconds of oxygen starvation that can stem from very rapid umbilical cord clamping— practices for which have changed (more rapid clamping has been adopted) over the past several decades.

It is difficult for an outsider to evaluate this controversial literature, but in exploring it, I was struck by how primitive and incomplete this scientific subdiscipline is. One might imagine that we have a thorough understanding of the risks and advantages of simple variations in birthing. That is not the case. One might even imagine that natural birthing might provide a pretty good model of the “ideal”, but as in many aspects of medicine, science teaches us (evidently) that “we can do better”.

All WE know is that a few (and especially, many) tens of seconds of oxygen deprivation can almost certainly be expected to specifically compromise the anoxia-hypersensitive auditory neuroaxis, and that this will increase brain “noise” in a system that we know expresses signature deficits for autism (language development). Which clearly makes this a subject worthy of more serious, more sophisticated and more complete study.