Neurodevelopment and Onsets of Mental Illness including Depressions

Adolescence is a critical stage in the life course when approximately half of all adult mental illnesses emerge, with clinical depressions comprising the greatest incidence risk, yet we still know very little about how or why this occurs. Theories include psychosocial acceleration, epigenetic and genetic vulnerability, differences in the timing and rates of development occurring across regions of the brain (heterochronicity), dual-process models, and a glucocorticoid vulnerability cascade linked to early life stress. Does one of these theories better explain onsets of (i) episodic and (ii) sex-differentiated mental illnesses, including depressions, (iii) occurring in adolescence? We argue no and that, more likely, a confluence of these theories may be best when attempting to explain each of these three perplexing aspects of mental illness.