When inflammation torments the soul
Depression is a mental disorder that expresses itself through a variety of symptoms. In medicine, depression is divided into three groups:
The affective psychosis, which used to be called endogenous depression. Here the causes arise as a result of altered metabolic processes in the brain, which may have their origin in the genetic code. Neurotic depression (exhaustion depression), which occurs as a result of a long-lasting stress in one's life history.
And reactive depression, which occurs as a reaction to an acute severe experience.
Depression is divided into three levels of severity:
– Mild depression: two main symptoms and two additional symptoms – Moderate depression: two main symptoms and three to four additional symptoms – Severe depression: three main symptoms and five or more additional symptoms
In order to be able to classify the severity of a depression, there are the following groups of causes, which are of course supplemented by a variety of individual perceptions.
The main symptoms of depression are:
– depressed, depressive mood – loss of interest and joylessness – lack of drive with increased fatigability
In addition, there are other complaints (secondary symptoms) that may indicate depression:
– reduced concentration and attention – reduced self-esteem and self-confidence – feelings of guilt and worthlessness – exaggerated fears of the future or "seeing the black" – suicidal thoughts or attempts, self-injury – sleep disturbances – reduced appetite
Depression is a complex disorder that affects the body and psyche equally. According to recent neuroscientific findings, the body, specifically the immune system and the brain, plays an important role in the development of the disease pattern.
Researchers have been searching for causes of depression in various ways for some time now. Scientists have been able to provide increasing evidence that the origin of depression should not be located solely in the psyche. A neuroscience study at the Centre for Addiction and Mental Health (CAMH) in Toronto again shows an important link between inflammation of the brain and the intensity of a depressive disorder. As a result, the research team found 30% higher inflammatory parameters in the brain in people with clinical depression.
For Dr. For Mario Krause, this study is an important argument for broadening the medical perspective in practice. "Depression is just one disorder in a whole series of complex diseases for which the search for causes can make therapy more successful. Classically, medicine focuses on symptoms. Functional interactions in the complex interplay of body systems as possible causes for the development of diseases are generally not in focus. The latest study from Canada in particular highlights the role of the immune system in the development and progression of depression. The researchers' findings expand the possibilities of medicine. This should be reason enough to push ahead with causal research on the one hand and to expand therapies on the other."
In addition, according to scientific evidence, there is a link between stress and depression. Stress causes an increased release of cortisol in the body, putting a strain on the immune system. The longer the period of stress lasts, the more the body's sensitivity to elevated cortisol levels decreases. This in turn magnifies the influence of proinflammatory cytokines on the immune system and metabolism.
A holistic diagnosis and therapy, which for example examines metabolic disorders, includes lifestyle and takes environmental factors into account, offers a useful complement to a classical therapy approach not only for depression but also for many other clinical pictures.
Stress: immune response and depression (a)
Activation of NF-KB by Toll-like receptors (TLRs) leads to an inflammatory response that (b) triggers the release of the proinflammatory cytokines TNF-α, IL-1, and IL-6. (c) Cytokines have access to the brain, active transport molecules and afferent nerve fibers via leaky areas in the blood-brain barrier (z.B. sensory vagus) that relay information through the nucleus tractus solitarius (NTS). (d) In the brain, cytokines participate in signaling pathways (shown in orange) known to be involved in the development of depression.
(i) Altered metabolism of the neurotransmitters serotonin (5-HT) and dopamine (DA)
(ii) Activation of CRH and production and/or release of ACTH and glucocorticoids (cortisol)
(iii) Disruption of synaptic plasticity by changes in relevant growth factors [z.B. Brain-derived neurotrophic factor (BDNF)].
(e) Exposure to stressful environmental factors promotes activation of inflammatory signals (NF-kB) through increased proinflammatory responses of the nervous system [release of norepinephrine (NE) that binds α (αAR) and β (AR) adrenoceptors] (shown in orange). (f) Stressors block vagal entry [release of acetylcholine (ACh) that binds the α7-subunit of the nicotinic acetylcholine receptor (α7nAChR)] (shown in blue). (g) Activation of mitogen-activating proteins, including p38 and JNK. Glucocorticoid receptor (GR) function is inhibited. NF-kB is released by the negative regulation of glucocorticoids as a result of the free HPA axis. Is the brain's response to stress (shown in blue).
Source: Charles L. Raison, Lucile Capuron, and Andrew H. Miller: Cytokines sing the blues: inflammation and the pathogenesis of depression. In: Trends Immunol. January 2006; 27(1): S.