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I am most appreciative to all of the commentators for their investment of the time and energy required to engage with and respond to my lengthy and somewhat complex article with such interesting contributions. Three of the commentators Anne Alvarez, Bruce McEwen, and Jaak Panksepp responded by noting general agreement with my model and, then, from their own specific areas of experience, research, and expertise, made most helpful suggestions for both expanding various aspects of the model and for developing and enriching a truly integrative and multifaceted approach to treatment of ASD. Since this is exactly what I had hoped for, I found this quite encouraging. In contrast, my article evoked quite a different response from Lisa Ouss and Fabian Gunol. I am grateful that through addressing a limited number of their concerns, I have the opportunity to clarify aspects of my model that may have been unclear.
As is obvious from my article, I have relied heavily on McEwens ground-breaking work on stress, allostatic load, neuroplasticity and epigenetics in developing my model, and its implications for treatment. Thus, I am quite pleased by his positive response and appreciative of his further significant clarifications regarding these processes. Before considering his suggestions regarding treatment, I will address two areas which he raised: (1) sex differences in both frequency as well as strategies for treatment which, as he points out, are important areas that I did not consider and (2) the broader implications of my model for neuropsychiatric disorders beyond ASD.
Recently, sex differences in autism have become of increased investigative interest (Halladay et al., 2015; Singer, 2015). While the frequently stated male preponderance in autism, a ratio of 4:1, has begun to be questioned on the basis of diagnostic differences between males and females, a biologically based sex difference in ASD prevalence remains, with a size of at least 2:13:1 (Halladay et al., 2015).