The minds habit of suppressing and avoiding intensely painful emotions may provide some temporary feelings of relief, but dissociation can also lead to unhealthy coping mechanisms, while simultaneously causing the side-effect of blocking out or blunting positive emotions, thereby reducing the access of people with BPD to the valuable information those emotions provide: information that helps to guide effective, healthy decision-making in daily life. Psychotic symptoms
Though BPD is primarily seen as a disorder of emotional regulation, psychotic symptoms are fairly common, with an estimated 21–54% prevalence in clinical BPD populations. These symptoms are sometimes referred to as "pseudo-psychotic" or "psychotic-like", terms that suggest a distinction from those seen in primary psychotic disorders. Recent research, however, has indicated that there is more similarity between pseudo-psychotic symptoms in BPD and "true" psychosis than originally thought. Some researchers critique the concept of pseudo-psychosis for, on top of weak construct validity, the implication that it is "not true" or "less severe", which could trivialize distress and serve as a barrier to diagnosis and treatment. Some researchers have suggested classifying these BPD symptoms as "true" psychosis, or even eliminating the distinction between pseudo-psychosis and true psychosis altogether.The DSM-5 recognizes transient paranoia that worsens in response to stress as a symptom of BPD. Studies have documented both hallucinations and delusions in BPD patients who lack another diagnosis that would better account for those symptoms. Phenomenologically, research suggests that auditory verbal hallucinations found in patients with BPD cannot be reliably distinguished from those seen in schizophrenia.
The HPA axis functions to maintain homeostasis when the body is exposed to stressors but has been found to be dysregulated among individuals with a history of childhood abuse. When the body is exposed to stress, the hypothalamus, specifically the paraventricular nucleus (PVN) releases peptides arginine vasopressin (AVP) and corticotropin-releasing factor (CRF). When these peptides travel through the body, they stimulate corticotrophic cells, resulting in the release of adrenocorticotropic hormone (ACTH). ACTH binds to receptors in the adrenal cortex, which stimulates the release of cortisol. Intracellular glucocorticoid receptor subtypes of mineralocorticoid receptor (MR) and low-affinity type receptor (GR) have been found to mediate the effects of cortisol on different areas of the body. While MRs have high affinity for cortisol and are highly saturated in response to stress, GRs have low affinity for cortisol and bind cortisol at high concentrations when an individual is exposed to a stressor. There have also been associations identified with FKBP5 polymorphisms, rs4713902 and rs9470079 in individuals with BPD. For those with BPD who have experienced childhood trauma, rs3798347-T and rs10947563-A have been associated, specifically in individuals with both BPD diagnosis and a history of childhood physical abuse and emotional neglect. Hypothalamic-pituitary-adrenal axis
The hypothalamic-pituitary-adrenal axis (HPA axis) regulates cortisol production, which is released in response to stress. Cortisol production tends to be elevated in people with BPD, indicating a hyperactive HPA axis in these individuals. This causes them to experience a greater biological stress response, which might explain their greater vulnerability to irritability.