Burnout: An excess on the axis

5. September 2011

Neuro-psychobiological stress research data provide new insights into the causes of burnout: In the etiological search for clues, unambiguous evidence is turning up which suggest that the hypothalamic-pituitary-adrenal-axis plays a key role.

It really doesn’t exist at all: one can search the current medical classification systems of ICD 10 and DSM IV for Burnout Syndrome in vain. But what “until now diagnostically has not existed” has, according to Prof. Dr. Wolf-Dieter Gerber (director of the Institute for Medical Psychology and Medical Sociology at the University Hospital Schleswig-Holstein, Campus Kiel) developed in recent years to become a common disease: “Almost thirty percent of the population suffers from fatigue, which leads, for many of those affected, to the decline of their professional and work capacities.” Alongside the medical psychologists and sociologists from Kiel, numerous other experts have declared a real “burnout-alarm”.

Hyperactivity in the HHNA

Hidden behind burnout – “the infarct of the soul” – at first one saw predominantly occupational stress factors, says Prof. Gerber. Especially in the ninteen-nineties, professional effort-reward imbalance and high work demands were blamed as essential causes. Only recently have neuro-psycho-biological aspects come into the focus as an explanation of the cause. Recent evidence from stress research shows, according to the words of Prof. Gerber, that the hypothalamic-pituitary-adrenal axis is an important etiopathogenetic factor: this second hormonal stress-axis – in short: HPAA – has been accorded in the origin of Burnout Syndrome a role of essential significance. The neuroendocrine control and feedback system modulates effects of stress by ensuring the demand-adjusted production and release of steroid hormones from the adrenal cortex. Persistent exposure to stress allows the regulation of the hormonal stress response, however, to derail. Chronic stress leads, according to Prof. Gerber, “to a significant increase in the activity of HPAA and also increases its sensitivity, which has far-reaching consequences”.

Harmful processes already in the womb

The hyperactivity of the neuroendocrine stress axis, and the consequently faulty homeostasis of the stress hormone, puts the affected person into a continuous state of alert. This leads to increased long-term cortisol levels and its many negative effects, most notably including immunosuppression, loss of muscle and bone tissue and increased blood sugar levels. In addition, disturbances in the regulation mechanism of HPAA has effects directly on the central nervous system. To this extent, burnout, according to Prof. Gerber, is a “stress disease with central nervous system consequences.” Such has been shown in studies using, among other things, PET and MRI scans, where in burnout-patients the activity of the amygdala was found to be elevated. Beyond that, the volume of the hippocampus had shrunken.

These harmful processes can already be set in place in the womb, as was demonstrated in 1989 by British scientist Dr David Barker. The Barker Theory of so-called foetal programming also applies to the effects of stress. Prenatal maternal stress affects the brain of the foetus: In the course of “fetal programming”, activity of and sensitivity to HPAA are increased. Therefore an increased risk of mental illness in later life can be a hard-wired one, says Prof. Gerber. The path to an increased predisposition to burnout is thus paved before birth.

The stress response is also located in the genes

How strongly the neuroendocrine stress-axis responds to a stress stimulus is highly individually variable. Against this background there are currently, in the words of Prof. Gerber, “genetic factors also being discussed which determine the sensitivity of HPAA”. Being a consequence of inherited tendencies, gene polymorphism influences the reactivity of the stress-axis. In other words, the strength and capacity to regulate the neuroendocrine stress response is also genetically determined. This was, for example, demonstrated for a widely spread variant of the gene which encodes the mineralocorticoid receptor (MR). In carriers of this MR180V allele, the neuroendocrine response to a stressor is significantly greater than in those who do not possess this gene variant. In addition, a polymorphism of the BDNF gene, Val66Meta, with a direct influence on the reactivity of the HPAA, was also found.

Brain Derived Neurotrophic Factor (abbreviated BDNF) largely determines the synaptic plasticity of neurons. Such “stress genes” – gene polymorphisms which have an affect on the stress response – are found, according to Prof. Gerber, in thirty percent of the population. The vast majority of this group, about seventy percent, are women. These genes do not necessarily need have negative effects – as long as the management of stress, so-called “coping”, works. If this fails, the stress genes then can indeed, even with only low stress-loads, get switched on.

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