All of the following are true about the etiology of Post-Traumatic Stress Disorder (PTSD), except

Choice A reason: Previous psychiatric history increases PTSD risk, as pre-existing conditions like depression or anxiety indicate heightened amygdala sensitivity and dysregulated stress responses. These predispose individuals to exaggerated fear responses post-trauma, as the brain’s stress circuitry is already compromised, amplifying the impact of traumatic events on neural pathways. Choice B reason: PTSD is not associated only with personal characteristics; it requires exposure to a traumatic event, as defined by DSM-5 criteria. Trauma triggers neurobiological changes, including amygdala hyperactivity and hippocampal volume reduction, causing symptoms like flashbacks. Personal characteristics modulate risk, but event exposure is essential, making this statement false. Choice C reason: A causative trauma is required for PTSD, per DSM-5, involving exposure to actual or threatened death, serious injury, or sexual violence. This triggers neurobiological changes, such as elevated cortisol and amygdala activation, leading to intrusive memories and hyperarousal. This criterion is fundamental to the disorder’s pathophysiology and diagnosis. Choice D reason: Lack of social support increases PTSD risk, as it exacerbates stress responses by reducing oxytocin-mediated emotional regulation and prefrontal cortex modulation. Social isolation heightens amygdala activity, prolonging trauma-related symptoms. Support systems buffer stress responses, making this a scientifically valid factor in the etiology of PTSD.