A highly relevant risk condition

Burnout develops as a process. In most cases, patients only become acutely aware of decompensation. Multimodal integrated therapy is needed.

The first description of burnout symptoms by Herbert Freudenberger a good 40 years ago was based on self-observation. Since then, clinical diagnostic criteria and questionnaires have been developed such as the Maslach Burnout Inventory and the Shirom-Melamed Burnout Measure [1]. Burnout remains a clinical finding, especially since meaningful peripheral biomarkers are not yet available [2]. Exhaustion syndrome (burnout) is not classified as a separate psychiatric diagnosis in either ICD-10 or DSM-5 and is coded as an additional diagnosis (Z73.0). The main diagnosis then refers to the diagnostically overlapping symptoms of depression, anxiety and panic disorder, secondary dependency, somatoform disorder, sleep disorder, etc., which occur almost regularly in the course of burnout. This makes it difficult to determine the frequency of the burnout syndrome. Sick leave due to the diagnosis of burnout peaked in Germany in 2011/2012 and has been decreasing since then, while days of absence due to mental illness increased by 41% in the period 2011-2015 [3]. It can be assumed that the situation in Switzerland is similar. One rationale is that “mental illness caused by chronic stress is now more likely to be recognized as adjustment disorder or depression.” This gives reason to hope that the discussion will become more objective as the taboo surrounding mental disorders decreases and gives way to a “more open and differentiated approach” on the part of patients, physicians and in companies [3]. Nevertheless, burnout as a stress-induced risk state for mental disorder remains highly relevant clinically and socioeconomically.

The burnout syndrome as a stress-induced risk state

Burnout occurs due to a chronic stress load predominantly in the work environment, but also in the private environment. Individual stressors are demands that exceed the resources of the person’s work-related and social skills as well as personal resilience and cannot be controlled or rejected. They induce a permanent activation and deregulation of the stress system with processively increasing symptomatology, which can be explained by neurobiological changes:

Psychologically, activation of the limbic system and especially the amygdala results in a “continuous alarm” with high irritability [4], aggressiveness and combative exertion/perseverance or social withdrawal with social, fear of failure and illness, emotional lability, sensitivity to stimuli (e.g., tinnitus, dysesthesias), up to anhedonia with a feeling of emptiness and a risk of suicide.
Somatically, chronic sympathicotonic adrenergic activation increases heart rate and blood pressure as well as muscular tension. Increased cortisol secretion due to dysfunction of the hypothalamic-pituitary axis (HPA axis) increases blood clotting, blood glucose, triglyceride, and cortisol levels and increases the risk of cardiovascular disease, diabetes, and/or metabolic syndrome. Sleep onset and sleep maintenance disorders with a lack of deep sleep occur when parasympathetic-dominated rest phases are reduced and the nighttime cortisol level is too low. Lack of rest, daytime fatigue, increased sensitivity to pain (sleep deprivation lowers the pain threshold), and muscular tension favor the development of musculoskeletal pain syndromes. Cortisol-induced changes in immune defense with release of interleukins (IL-6, TNF-alpha) [5]. A feeling of illness similar to fatigue and a susceptibility to infections develop. In the course, relative hypocortisolism may develop favoring allergies and autoimmune diseases.
Cognitive performance declines under sleep deprivation and daytime sleepiness, as well as under the toxic effect of cortisol on hippocampal neurons. In addition, the sleep phases that the hippocampus needs to store memory content are missing. Stress also leads to alteration of neurotrophic factors such as “brain derived neurotrophic factor” (BDNF) and “cyclic AMP response element-binding protein” (CREB), which influence individual CNS plasticity [6].

Risk and resilience factors

Work-related risk factors at the organizational level arise when there is a chronic mismatch between the quantitative and, in particular, qualitative demands and resources of work, e.g. simultaneously high responsibility, time pressure and psycho-physical stress on the one hand and too few opportunities for control and influence, recognition, social support and job security on the other. “Gratification crises” according to Siegrist [7] arise subjectively perceived from the imbalance of one’s own effort and return.

Increased stress sensitivity as a neurobiological vulnerability already arises pre- and postnatally due to genetic and epigenetic predisposition and imprinting. A large Swedish twin study was able to prove the importance of genetic predisposition for the development of burnout. Among these, 38% of the variance in burnout is explained by additive genetic influences (compared to 45% in major depression and 49% in generalized anxiety disorder) [8]. Gene variants (e.g., of the FKB5 gene), polymorphisms (e.g., truncated variants of the serotonin transporter promoter gene), or DNA methylation of the glucocorticoid receptor gene (NR3C1) are associated with dysregulation of the HPA axis as well as increased rates of depression and chronic stress [2]. The stress processing system of the fetus develops in response to the level of cortisol in maternal blood in analogy to the mother’s stress and stress processing [9]. Inactivation of the glucocorticoid receptor gene due to increased methylation causes a persistent – but in principle reversible – overactivation of the stress hormone axis.

Postpartum, early childhood attachment experiences have the most important influence on the further development of stress processing. Ambivalent or anxious-uncertain attachment, especially dismissive-critical parenting behavior, increases dysregulation of the stress hormone axis, whereas secure attachment has a compensatory effect [10]. Animal studies suggest reversibility of genetic-epigenetic changes under favorable conditions of an “enriched environment” also in adult mice [11].

The individual sensitivity of the stress axis, together with the attachment experiences (or possible traumas), forms the basis for personal resilience. The ability to process stress, to tolerate it and to be able to calm down is crucial. Essential skills are self-awareness, self-regulation, and self-care.

Good resilience is based on basic security, self-confidence and self-acceptance (with the integration of mistakes and weaknesses) and a sense of self-efficacy as well as social competence, distancing and conflict skills.

A higher risk of burnout is seen in people with ambivalent, anxious-insecure attachment style, vulnerable narcissistic regulation with unstable self-esteem, high striving for perfection and recognition, high sickliness and lack of social interaction and conflict ability, willingness to spend up to an altruistic self-sacrificing attitude with control desires or a resignative-avoiding withdrawal [12,13].

In the working population, burnout is strongly associated with alexithymia [14]. Our own unpublished data show alexithymia 3.5 times more often in patients with burnout than in the general population. This can be acquired in early childhood, but may also have been trained under chronic stress as a defense, protection and success factor and then often decompensates in somatoform complaints, hypochondria and fear of illness.

Therapy and prevention of burnout

Burnout develops in a process. However, decompensation is usually felt acutely and violently by the patient. Starting therapy in an outpatient setting can be attempted for moderate/severe burnout with psychological and somatic comorbidity, but often the exhausted patient is overwhelmed by the necessary combination of talk, relaxation, and sports therapies. Therefore, treatment in a holding inpatient setting can be recommended at an early stage, always with the aim of continuing outpatient therapy to accompany the gradual vocational reintegration already prepared in the inpatient setting.

Elements of inpatient integrative psychosomatic therapy are psychotherapy in individual settings as well as in interactive and psychoeducational groups with distancing from the stressful situation, de-anxiety with regard to the symptomatology, strengthening of emotional and physical self-perception, self-regulation and self-efficacy as well as improvement of skills of perception of others, change of perspective and social training.

Psychovegetative stabilization is sustainably supported by learned relaxation methods (Qigong, Yoga, PMR, etc.), mindfulness is practiced as an attitude. Adapted endurance, strength and coordination training, dance therapy and revitalization of individual resources related to nature experience, creativity and social contacts make corrective experiences possible. Exercising procedures are used in a targeted manner. Couple and employer meetings are usually required. Socially, the group of therapists and patients represents a training ground for the implementation of newly acquired possibilities of behavior and communication. Catamnesis studies suggest that treatment of burnout can be successfully sustained despite the importance of personality factors [12,13].

Take-Home Messages

Burnout develops as a process. In most cases, patients first become acutely aware of decompensation.
Individual risk and resilience factors are determined psychologically (e.g., personality factors) and biologically (e.g., epigenetic).
Burnout is a risk condition for psychiatric, cardiovascular, metabolic, and pain disorders. Multimodal integrated therapy of the psychological, cognitive and somatic aspects is needed.
Improving the ability of psycho-physical stabilization, self-awareness and self-regulation, self-care and social skills is important for individual prevention and treatment.

Literature:

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Bakusic J, et al: Stress, burnout and depression: A systematic review on DNA methylation mechanisms. J Psychosom Res 2017; 92: 34-44.
Deutsche Angestelltenkrankenkasse: DAK Health Report 2016. www.dak.de/dak/bundes-themen/burnout-rueckgang-1806804.html
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