Why don't we talk about depression

That is why depression is not an imagination

The oldest and at the same time best known theory about the biological processes in the brain during depression is the monoamine deficiency hypothesis. A core element of this hypothesis are the messenger substances via which nerves in the brain communicate. These so-called neurotransmitters belong to the chemical group of monoamines.

This is how communication works in the brain

To understand exactly what this all means, a short excursion into the way the brain communicates: The nerves in the brain consist of a cell body, an axon and the synaptic endbones. You can imagine it like a little tree. The end knobs are the roots in the earth, the axon is the trunk and the cell body is the tree crown.

Nerve cells specialize in exchanging information. They communicate using both electrical and chemical signals. When a nerve cell is activated, it conducts an electrical signal through its axon. When it arrives at the synaptic end knobs, the voltage triggers the release of chemical substances: the neurotransmitters. The neurotransmitters can be used to bridge the gap to the next cell. One nerve cell can communicate with the other in this way,

The opposite ends of the two nerves, along with the space between them, are known as the synapse. When the concentration of neurotransmitters in the synaptic gap (the space in between) increases, the messenger substances begin to bind to the receptors on the outer walls of the cell. This can have both an activating and an inhibiting effect. In the event of an activation, the signal is passed on; in the event of an inhibitory effect, it is suppressed.

If communication does not work properly, depression can occur

Normally, these processes take place at the synapses in such a way that feelings, thoughts and movements can be properly passed on in the brain. However, if parts of the complex system get out of hand, this can contribute to the development of depression, according to the monoamine deficiency hypothesis. For example, when the receptors on the outer walls of the nerve cells do not function properly and the transmitters are pumped back into the cell too quickly. Or if there are already problems with the production of the messenger substances inside the nerve cell, or if the nerve cells are over-sensitive or resistant to the messenger substances.

The name monoamine deficiency hypothesis specifically refers to the fact that certain synapses do not have enough messenger substances to ensure the smooth transmission of information. This can have genetic causes, but it doesn't have to be.

The symptoms of those affected differ

It becomes even more complex because there is not just one but many different messenger substances. Serotonin and norepinephrine are particularly well known. The symptoms of those affected differ depending on which signal chain is disturbed. Based on this, depression is treated with various antidepressants. The drugs are mostly aimed at increasing the concentration of the messenger substances in the synaptic gap and thereby getting the communication between the nerves back on track. For example, by suppressing the re-uptake of serotonin in the synaptic endnaps.

There are doubts about the hypothesis

There are many people for whom treatment with antidepressants does not work even after several attempts. They are called "treatment-resistant". Because of these patients, too, doubts about the monoamine deficiency hypothesis are repeatedly raised. It is clear that this approach alone is not enough to explain the development of depression.

The brain's ability to regenerate could be restricted

Other explanations therefore focus on the interaction between the brain and the general state of health of a person.
Studies have shown that a particular area of ​​the brain called the hippocampus is below average in size in some people with depression. This has led to the hypothesis that nerve growth may be restricted in depressed people. This would also reduce the number of synapses.

Chronic stress can be a trigger for depression

People who are depressed often have elevated cortisol levels. In animal studies and in humans it has also been shown that the feedback mechanism, via which stress reactions in the body are downregulated, sometimes no longer works properly after traumatic experiences. This leads to a permanent release of stress factors, which in turn inhibits nerve growth in the brain. This could explain how long-term stress or trauma contribute to depression.

Antidepressants usually have a delayed effect

This theory is supported by the fact that antidepressants have a positive effect on the regulation of the stress response in the body and stimulate nerve growth. An explanation that fits in with the typically delayed effects of antidepressants. Because although the drugs increase the availability of the messenger substances in the synaptic cleft within a few hours or days, those affected only feel the positive effect after three or four weeks.

Contrary to the theory, there are no signs of overactivation of the stress response in most patients with depression. However, it is just as difficult to find concrete, solid evidence for the monoamine deficiency hypothesis.

Inflammation in the body leads to inflammation in the brain

The immune system could also be related to depression. Animal studies have shown that chronic inflammation in the body can spread to the brain. There are special immune cells there, the microglia. Chronically elevated inflammatory factors can overactivate the microglia cells. This can also lead to the death of nerve cells via complex signal chains and many intermediate steps.