April 22, 2024

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What are “dangerous factors” in the brains of patients with depression?

What are “dangerous factors” in the brains of patients with depression?

What are “dangerous factors” in the brains of patients with depression?

According to a survey conducted in 2023 targeting 100,000 Japanese individuals, a staggering 78.5% of respondents answered that they felt “tired.”

However, in the West, “working while tired” is considered a sloppy behavior due to the inability to manage oneself, leading to the scientific study of fatigue being overlooked.

In Japan, where “fatigue” is considered a virtue, and people praise each other with “otsukaresama” (thank you for your hard work), research on fatigue is leading the world. The author leading fatigue research in Japan has achieved numerous Nobel Prize-worthy new studies, revealing the surprising reality of fatigue.

In the previous chapter, as mentioned in the explanation of chronic fatigue syndrome, discussing the mechanism of disease onset without knowing the cause is futile.

However, fortunately, we have recently discovered genes that are believed to be risk factors for causing depression, which are produced when HHV-6 is latently infected in the host’s body. We have named this gene “SITH-1.” SITH-1 is pronounced as “Shisuwan.” The origin of the name will be explained later.

When we examined whether patients with depression have antibodies produced in response to the protein created by SITH-1, about 80% of patients with depression tested positive. And it was found that the susceptibility to depression in cases of positivity is as much as 12.2 times higher than in cases of negativity.

Scientifically, when a factor is considered one of the causes, it is more accurate to call it a “risk factor” rather than simply a “cause.” However, this number is so high that it is not an exaggeration to say that “SITH-1 is the cause of depression.”

In the pathological fatigue of chronic fatigue syndrome, the problem of “unknown cause” has hindered the elucidation of the onset mechanism. However, with the discovery of SITH-1, there is growing hope that discussions overcoming this problem may be possible in the case of pathological fatigue in depression.

In conclusion, it has been found that by elucidating how SITH-1 brings about pathological fatigue, the problem of depression can be significantly resolved. In this chapter, we will explain the relationship between SITH-1 and depression, such as how we discovered SITH-1 and why it is considered a cause of depression, in chronological order.

(Note) Depression is referred to as “major depression” when expressed as a disease name. However, in this book, the word “depression” is used to describe a broader meaning than “major depression,” and it explains depression in a broad sense that is not limited to major depression.

What are "dangerous factors" in the brains of patients with depression?

What are “dangerous factors” in the brains of patients with depression?

What is depression in the first place?

To understand why SITH-1 causes depression, it is necessary to know what is happening in the brains of patients with depression. But before that, we need to know what depression is in the first place.

The definition of depression, or diagnostic criteria, is basically as follows.

First, one of the following is essential:

  • Feeling depressed almost all day
  • Feeling no interest or pleasure in almost all activities almost all day

Next, the following secondary symptoms are:

  • Decreased or increased appetite
  • Insomnia or hypersomnia
  • Psychomotor agitation or retardation
  • Fatigue or loss of energy
  • Feelings of worthlessness or excessive guilt
  • Diminished ability to think or concentrate
  • Recurrent thoughts of death

If five or more of these symptoms persist for two weeks, depression is suspected.

Also, it is a condition that excludes other diseases.

Although the criteria are quite strict, it is evident from these diagnostic criteria that depression is not something that can be attributed to a single cause.

Moreover, there are no examination items in these diagnostic criteria.

Due to the unknown cause, each researcher studying depression does not even know if they are really studying the same disease, similar to chronic fatigue syndrome.

Nevertheless, in the process of searching for the cause of depression, little by little, what depression is as a disease and what is happening in the brains of patients with depression have become clearer.

First, let’s look at the main theories regarding the cause of depression and what is happening in the brains of patients with depression.

What is happening in the brains of patients with depression?

Psychogenic theory This theory is not so much that the cause of depression is a psychological problem, but rather that depression is not a disease in the first place.

The feelings of depression and loss of pleasure that occur in depression are due to deep thinking, which is a personality trait, and not an illness.

When it comes to great minds with depression, in Japan, there are writers like Ryunosuke Akutagawa and Osamu Dazai, and internationally, there are great geniuses like Charles Darwin, who developed the theory of evolution, and mathematician Georg Cantor, and many others.

The psychogenic theory is not an outdated idea, and there are still many doctors who adhere to it. Such people, when introducing their hospitals on the internet, emphasize that they use treatments that do not involve drugs as much as possible.

According to the psychogenic theory, even if a person becomes depressed, the brain of the patient does not fundamentally change.

What is happening in the brains of patients with depression?

Monoamine theory and serotonin theory Among the neurotransmitters working in the brain, dopamine, norepinephrine, and serotonin, collectively referred to as “monoamines,” have the function of enhancing brain function and elevating mood. The “monoamine theory” of depression suggests that depression occurs due to a deficiency of monoamines in the brain.

The beginning of this theory was the discovery that patients with tuberculosis who were administered the anti-tuberculosis drug iproniazid became excited or cheerful. Upon investigation, it was found that this drug inhibits monoamine oxidase, which inhibits the breakdown of monoamines, thereby increasing the concentration of monoamines in the brain.

Therefore, it was thought that the decrease in brain monoamine levels might be the cause of depression, and various antidepressant drugs that increase brain monoamine levels were developed.

Eventually, it was found that among these antidepressant drugs, a class of drugs called selective serotonin reuptake inhibitors (SSRIs), which selectively increase the level of serotonin, showed even higher antidepressant effects. Therefore, it was suggested that the cause of depression is a deficiency of serotonin in the brain. This is the “serotonin hypothesis.”

However, it is now believed that both the monoamine hypothesis and the serotonin hypothesis are incorrect as explanations for the cause of depression.

The first reason is that these drugs take 2 weeks to 1 month to show their antidepressant effects after administration. If a deficiency of monoamines such as serotonin is the cause of depression, it would be strange if there were no immediate effects after administration.

The second reason is that even when the brains of patients with depression are examined, there is no evidence that there is a deficiency of monoamines such as serotonin.

However, these antidepressant drugs are very effective in at least half of patients with depression. Therefore, they must be playing some role. There are several hypotheses, such as the hypothesis that monoamines and serotonin elevate mood when they are excessive, and the hypothesis that SSRIs have neurotrophic effects and repair neurons that are functioning poorly in patients with depression.

However, in any case, it seems that none of these hypotheses reveal how the brains of patients with depression are changing.

What is happening in the brains of patients with depression?

Brain inflammation theory The most likely cause of depression at the moment is considered to be inflammation of the brain, particularly the hyperproduction of inflammatory cytokines by glial cells involved in brain immune function, such as microglia and astrocytes.

This theory originally stemmed from the observation that phenomena such as depression are observed at a high frequency in people with persistent inflammation in the peripheral parts of the body, such as rheumatism and infections. From this, it was thought that depression might occur because inflammatory cytokines act on the brain.

When you hear that, you might think, “Wait, I’ve heard this somewhere before.” Yes, this is the same mechanism as the one explained in Chapter 1, where fatigue occurs due to physiological fatigue, and although there is a difference in whether inflammation occurs in the periphery or in the brain, the mechanism is the same. Then why does one become “depression” and the other remain as “fatigue”? The answer to this question is expected to lead to the prevention and treatment of depression, and this book also has the goal of finding the answer to this question. However, the road to that answer is not easy, so we will gradually clarify it from now on.

Returning to the original topic.

The theory that brain inflammation is the cause of depression is considered almost certain based on many examinations, such as investigations of the brains of deceased patients with depression, PET (Positron Emission Tomography) examinations of patients with depression, and experimental results in animals in which inflammation was experimentally induced in the brain.

Then, the problem of what is the cause of depression is narrowed down to the question of what is the cause of brain inflammation in patients with depression.

Furthermore, the serial article <Japan is actually leading the world in “fatigue research”… “Fatigue” and “feeling fatigued” are different> will continue to explain fatigue in detail.

What are “dangerous factors” in the brains of patients with depression?

What are “dangerous factors” in the brains of patients with depression?

(source:internet, reference only)

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