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Consistent with the diathesis-stress model, the two-hit hypothesis ( i.e ., early genetic and environmental discrepancies produce long-term vulnerability to a “second stress hit” that leads to the emergence of symptomatology) and its meta-evolved three-hit hypothesis ( i.e ., hit-1: genetic predisposition, hit-2: early-life environment, and hit-3: later-life environment) suggest that, in a given environmental context, vulnerability is enhanced and symptomatology emerges when failure to cope with adversity accumulates [169, 170]

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