You know how it feels when you’re stressed, right? And you can certainly imagine that stress is not just a subjective experience but also depends heavily on bodily processes and hormones. However, it’s quite important to mention that stress affects individuals differently – and some people presumably more than others.
Accordingly, research suggested that individuals with Borderline Personality Disorder (BPD) are particularly prone to feeling stressed out and corresponding studies imply that BPD symptoms can be categorized as chronic or acute stress-related symptoms. Chronic symptoms refer to stable and temperamental features such as dysphoria, intolerance of aloneness, and concerns of abandonment. Acute symptoms refer to spontaneous reactions to stress such as impulsive behaviors, sudden mood swings, and self-injury. Basically, however, BPD is characterized by affective instability, impulsivity, and interpersonal instability and can be diagnosed if five out of nine diagnostic criteria are met. And, the ensuing variety of symptom combinations leads to a heterogeneous clinical picture. But interestingly, altered stress sensitivity applies to the vast majority of BPD patients.
And while stress usually affects how you feel and how you behave, research suggested that stress levels can also be inferred from hormonal levels. Especially hormones of the so-called hypothalamic-pituitary-adrenal (HPA) axis play an important role when coping with stressful situations. Simply put, the HPA axis enables adequate reactions to stress through increased cortisol release, which is the best-known hormone of the HPA axis. Cortisol also restores homeostasis after stressful situations through downregulation of the HPA axis. And interestingly, various studies indicate that changed HPA axis functioning is closely associated with several clinical disorders such as depression or trauma. Taken together – and owing to existing links between altered neurobiological stress sensitivity and psychopathology – our group wondered whether altered stress sensitivity can be derived from neurobiological mechanisms in BPD, as well.
To systematically investigate this issue, we analyzed 37 studies on HPA axis functioning in BPD patients as compared to healthy and clinical control participants. And since HPA axis functioning depends on a large number of factors, we also checked if cortisol profiles differed depending on the testing procedures involved. For instance, we analyzed if cortisol patterns were altered when using one-time measurements as compared to repeated measurements. Additionally, we examined if cortisol patterns in BPD patients were abnormal in stressful social situations or after administration of pharmacological treatments, which usually suppress HPA axis functioning. Also, we investigated differences between studies using different sampling materials (i.e. saliva or blood) as well as studies of varying quality to determine the HPA axis profile in BPD as precisely as possible.
So, what would you expect – can stress levels be inferred from hormones? And are these hormones fundamentally different in BPD patients? According to our findings, both questions can be answered with “yes”. However, things aren’t that simple when taking a closer look. Basically, BPD patients display higher stress levels, thus elevated cortisol output, during the course of a day. Yet, in stressful social situations, cortisol profiles of BPD patients are blunted. Put differently, situations such as conflict discussions with relatives or job interviews seem to be less stressful for BPD patients. So taken together, the HPA axes of BPD patients release more cortisol on the whole but less when being in stressful social situations – and existing research may help to understand these patterns. On the one hand, BPD patients may be stressed more by little things in everyday life. And, as a result, BPD patients may respond with increased cortisol output. This would, for instance, explain why impulsive behaviors and self-harm are all too frequent in BPD – namely because it’s quite difficult to deal with a lot of stress constantly.
On the other hand, it might be reasonable to react with a certain stress level if there is a conflict at hand in order to focus attention on the specific situation. Optimally, this reaction should be reactive, so that there is a cortisol increase during stress and a decrease after the stressor has disappeared. However, and in contrast to the aforementioned stereotypical reaction, cortisol responses in BPD patients are generally lower than those of healthy individuals, which could indicate a lack of HPA axis reactivity. And, prior research explained these blunted cortisol reactions by a changed development of the HPA axis due to childhood trauma. Hence, everyday social difficulties may no longer influence cortisol patterns in BPD patients due to extreme and dysfunctional cortisol responses in early childhood. Put another way, traumatic experiences in childhood may lead to a so-called “burn-out” of the HPA axis in BPD patients. This does not imply that all BPD patients have had traumatic experiences but suggests that traumatic experiences in childhood play an important role in HPA axis functioning over the life span. However, more longitudinal research on potential links between stress and trauma in BPD patients is needed before drawing causal conclusions.
And last but not least, we found no differences when analyzing one-time cortisol measurements and measurements based on pharmacological challenges. We hypothesized that these methods are not sensitive enough when investigating cortisol patterns in BPD patients. However, at the present time, it is difficult to say whether these cortisol profiles are non-specific due to the testing procedures or due to the HPA axis profiles of BPD patients. Nonetheless, and owing to a remarkable potential of stress hormones for prevention and treatment research, it is much to be hoped that additional research examines HPA axis functioning of BPD patients as closely as possible.