Preprint Concept Paper Version 2 Preserved in Portico This version is not peer-reviewed

A Molecular Framework for Autistic Experiences: Mitochondrial Allostatic Load as A Mediator between Autism and Psychopathology

Version 1 : Received: 18 May 2022 / Approved: 21 May 2022 / Online: 21 May 2022 (10:53:46 CEST)
Version 2 : Received: 3 September 2022 / Approved: 5 September 2022 / Online: 5 September 2022 (03:35:24 CEST)

A peer-reviewed article of this Preprint also exists.

Mahony C and O’Ryan C (2022) A molecular framework for autistic experiences: Mitochondrial allostatic load as a mediator between autism and psychopathology. Front. Psychiatry 13:985713. doi: 10.3389/fpsyt.2022.985713 Mahony C and O’Ryan C (2022) A molecular framework for autistic experiences: Mitochondrial allostatic load as a mediator between autism and psychopathology. Front. Psychiatry 13:985713. doi: 10.3389/fpsyt.2022.985713

Abstract

Molecular autism research is evolving towards a biopsychosocial framework that is more informed by autistic experiences. In this context, research aims are moving away from correcting external autistic behaviors and towards alleviating internal distress. Autism Spectrum Conditions (ASCs) are associated with high rates of depression, suicidality and other comorbid psychopathologies, but this relationship is poorly understood. Here, we integrate emerging characterizations of internal autistic experiences within a molecular framework to yield insight into the prevalence of psychopathology in ASC. We demonstrate that descriptions of social camouflaging and autistic burnout resonate closely with the accepted definitions for early life stress (ELS) and chronic adolescent stress (CAS). We propose that social camouflaging could be considered a distinct form of CAS that contributes to allostatic overload, culminating in a pathophysiological state that is experienced as autistic burnout. Autistic burnout is thought to contribute to psychopathology via psychological and physiological mechanisms, but these remain largely unexplored by molecular researchers. Building on converging fields in molecular neuroscience, we discuss the substantial evidence implicating mitochondrial dysfunction in ASC to propose a novel role for mitochondrial allostatic load in the relationship between autism and psychopathology. An interplay between mitochondrial, neuroimmune and neuroendocrine signaling is increasingly implicated in stress-related psychopathologies, and these molecular players are also associated with neurodevelopmental, neurophysiological and neurochemical aspects of ASC etiology. Together, this suggests an increased exposure and underlying molecular susceptibility to ELS that increases the risk of psychopathology in ASC. This article describes an integrative framework shaped by autistic experiences that highlights novel avenues for molecular research into mechanisms that directly affect the quality of life and well-being of autistic individuals. Moreover, this framework emphasizes the need for increased access to diagnoses, accommodations, and resources to improve mental health outcomes in autism.

Keywords

autism; autistic burnout; social camouflaging; early life stress; suicidality; psychopathology; mitochondrial allostatic load

Subject

Medicine and Pharmacology, Neuroscience and Neurology

Comments (1)

Comment 1
Received: 5 September 2022
Commenter: Caitlyn Mahony
Commenter's Conflict of Interests: Author
Comment: The manuscript has been edited for length, clarity and cohesion. No major changes have been made to the content but some essential points of clarification have been added or rephrased where necessary.
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