Distress theory of depression: what it is, and how it explains this disorder.

An explanation of depression centered on inflammatory processes.

In Spain, more than 2.4 million people suffer from depression on a daily basis, which means that more than 5.2% of the Spanish population lives with a feeling of anguish and acute sadness that interferes or makes it impossible to live their lives normally.

Despite the high incidence of this disorder or emotional condition, there are still great disagreements within the scientific community as to its true cause. One of these theories is the malaise theory of depression, which we will explain below.which we explain throughout this article.

What is the malaise theory of depression?

Also known as the inflammatory theory of depression, this explanatory model of endogenous depressive disorders created by UK physician and researcher Bruce G. Charlton created by the United Kingdom physician and researcher Bruce G. Charlton in 2000, attempts to explain the origin of depression from a physical or organic point of view and not as a psychological reaction.

This theory begins with the idea that when our body is the victim of some kind of infection, our own organism emits an inflammatory response, by which an inflammatory response through which a series of hemodynamic alterations, lymphatic levels and the release of a series of agents such as cytokines, histamine, neuropeptides, etc., are carried out in order to restore the health of our body.

In addition, along with inflammation a psychological phenomenon known as Sickness Behavior appears.. This type of psychological response is characterized because the person experiences a series of sensations of tiredness, drowsiness, anhedonia and cognitive alterations, all this symptomatology coincides with part of the clinical picture of major depression.

The origin of this sickness behavior would be found in the effects that certain proteins, specifically cytokines, whose levels increase when a virus or infection appears, cause in our brain.

This association between physical or organic inflammatory response and psychological response is suggested by the theory of malaise. According to this theory, endogenous depression is a pathological variety of sickness behavior. Whereby the symptoms remain over time. Therefore, according to this theory depression is caused by the effects of chronic, low-level organic inflation and chronic activation of the immune system.

Finally, Charlton himself proposes that the true effect of Antidepressant drugs in alleviating the symptoms of the disease is to be found in the analgesic effect of the antidepressant drugs. is found in the analgesic effect that most of them have, so that by reducing organic inflammation, they also reduce the symptoms of depression.

On what evidence is this explanation based?

Although at first it may be somewhat difficult to believe that depression is not caused by an external factor that provokes this response, the discomfort theory is based on a series of empirical evidences that support it.

1. Coincidence of symptoms

As mentioned above, the symptoms of major depression coincide in many respects with those of sickness behavior, which tends to appear when we suffer from some kind of physical illness.

In these cases symptoms such as fatigue, decreased physical energy or feelings of anguish and sadness appear in order to keep our body at rest and recover as soon as possible. appear with the aim of keeping our body at rest and recovering as soon as possible.

2. The effect of cytokines

One of the physiological responses that our body provokes in the face of the threat of illness is the increase of cytokines. This protein provokes inflammation with the intention of transmitting to our organism that it is in a state of alert or threat.

If we take into account that, usually, in disorders with depressive symptomatology the levels of cytokines are much higher than usual, we can hypothesize a kind of relationship between these two factors.

Moreover, in the specific case of bipolar disorder, cytokine levels decrease during episodes of mania or remission of depressive symptoms, so this reinforces this hypothesis.This therefore reinforces this association.

3. Action of antidepressants

Antidepressant drugs have an effect on cytokine levels, specifically by decreasing them. This therefore reinforces the idea that the main cause of endogenous depression is to be found in the effects that these proteins cause in the organism.

4. The inflammatory response system and depression

Some studies have shown that laboratory inoculation with inflammatory substances or agents, causes a series of symptoms characteristic of clinical pictures of depression and anxiety..

In addition, a clear relationship has been established between the activation of the inflammatory response system of our organism and depression; since this system is continuously activated during this disorder.

The inflammatory response system works through the activation of the hypothalamic-pituitary-adrenal axis, which affects the regulation of certain neurotransmitters such as serotonin and catecholamines, directly related to depressive states.

5. Antidepressant action of anti-inflammatory drugs

Finally, some research has found that the administration of anti-inflammatory medication in some cases of endogenous depression not only significantly improves the symptoms of depression, but also does so to a greater extent than some antidepressants.

What if there is depression but no inflammatory disease?

The main criticism of the explanatory model of the malaise theory of depression is that there are a large number of cases in which it has not been possible to find a physical cause or a sign of organic inflammation in the patient. or sign of organic inflammation in the patient.

However, according to this theory it is argued that psychological stress processes can cause this inflammation just as any type of infection does, thus causing the symptoms of depression.

Experiencing high levels of stress over a long period of time has been linked to increased levels of proinflammatory cytokines. Which, as explained above, have a direct effect on serotonin levels and other neurotransmitters related to depression.