🌶️ 🧠 + masking= mitochondrial disfunction
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TLDR version from article :
An integrative biopsychosocial vulnerability framework for the development of psychopathology in ASC (created with BioRender.com). There is a well-established relationship between exposure to early life stress (ELS) or chronic adolescent stress (CAS) and the development of psychopathology. Autism is associated with both a significantly increased risk of exposure to ELS and high rates of psychopathology and suicidality. Emerging characterizations of internal autistic experiences including social camouflaging and autistic burnout overlap closely with established definitions for ELS and lead to increased levels of anxiety, depression, self-injury and suicidality in ASC. Thus, the development of psychopathology in autism may be mediated by an increased exposure to toxic stressors culminating in allostatic overload. Molecular stress research has demonstrated that mitochondrial allostatic load (MAL) plays a central role in psychopathology following ELS by disrupting a closely coupled network between neuroimmune and neuroendocrine signaling. Cellular neuroscience has comprehensively characterized the tightly regulated biochemical relationships between (i) mitochondrial dysfunction and neuroinflammation, (ii) mitochondrial metabolism and the HPA axis, and (iii) inflammatory- and HPA-signaling. Notably, ASC etiology is also characterized by mitochondrial dysfunction, gliosis and neuroinflammation, and a complex signature of HPA axis dysregulation. Moreover, this three-way molecular interplay converges on the regulation of key neurodevelopmental processes implicated in the response to ELS and psychopathology that are also associated with distinct neurophysiological, neurochemical and behavioral aspects of ASC etiology. Collectively, this could point to a molecular vulnerability to the development of psychopathology in ASC, highlighting how psychosocial and biological factors converge to increase the risk of psychopathology and suicidality.
Link to article
https://pmc.ncbi.nlm.nih.gov/articles/PMC9732262/
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