Is Oxidative Stress a Shared Mechanism Linking Autism Regression, Late Diagnosis, and Sex-Disparate Diagnostic Timing?

Autism spectrum disorder (ASD) research has largely treated early regression, late decline after a period of stability, gradual increases in symptom severity, late diagnosis, and the sex difference in diagnostic timing as separate topics. These phenomena differ in definition, evidence, and plausible mechanism, and diagnostic and recognition processes may explain much of the late-diagnosis and sex-timing findings. This narrative, hypothesis-generating review asks whether a cumulative oxidative and inflammatory burden, arising from environmental chemical exposure, infection and autoimmune activity, and chronic psychosocial stress, and modified by genetic susceptibility, one-carbon metabolism, the gut microbiome, and individual buffering capacity, could contribute to some of these trajectories. We grade the evidence for each link in four tiers (human ASD data, other human data, experimental models, and our hypotheses). Most links rest on associations with ASD risk or on experimental data; no study has linked these exposures to regression or late diagnosis, and oxidative stress may be a consequence or correlate rather than a cause. We therefore define operational terms, derive predictions that could refute the model, and outline the prospective, sex-stratified evidence needed to test it.