Is it possible to inherit depression - mood in genes

Endogenous depression is a very common mental illness, the main symptoms of which are depressed mood, motor slowing and inhibited thinking. Very often it develops in the midst of complete well-being and deals an irreparable blow both to the person himself and to his relationships with his family, to his work and hobbies.

Causes of endogenous depression and risk factors

The mechanism of development of the disease is not well understood. It is assumed that the cause of endogenous depression may be a violation of metabolic processes in the brain, namely a violation of the production of norepinephrine and serotonin.

Norepinephrine, called the “wakefulness mediator,” is a hormone of the adrenal medulla, belongs to the biogenic amines of the catecholamine group, takes part in the regulation of peripheral vascular resistance and blood pressure, and causes an increase in cardiac output. Serotonin, also called the “happiness hormone,” belongs to the tryptamine class of biogenic amines and plays the role of a neurotransmitter in the central nervous system. It facilitates motor activity, takes part in the regulation of vascular tone, affects the reproductive system, etc. The synthesis and metabolic processes of norepinephrine and serotonin have a certain connection.

People with certain character traits and personal qualities (hyper-responsibility, perfectionism, workaholism, increased sense of duty, suspiciousness, anxiety) have a tendency to develop endogenous depression.

Patients are recommended to practice yoga, take vitamin and mineral complexes, and take long walks in the fresh air.

Risk factors include:

• hereditary predisposition;
• chronic somatic diseases;
• metabolic disorders;
• age-related changes;
• physical and mental stress;
• poor nutrition;
• taking a number of medications;
• systematic vigorous activity at night;
• irregular work schedule and other occupational hazards.

Is there a gene that causes depression?

There is no specific gene that causes depression in humans. However, according to geneticists, there are several specific genes that, if you inherit them, increase your chances of suffering from depression. For example, if one parent suffers from depression, there is a 20-30% chance that you will inherit this predisposition.

Scientists are confident that genes influence our tendency to depression, but do not rule out that other factors are also an important component of a person’s general psychological state.

They studied pairs of twins to find out what role heredity plays in the development of depression. Research shows that heredity affects how your genes respond to various factors. The twins were chosen because they have the same set of genes (except for variables).

100 years ago, small towns in the USA looked unusual: historical photos

Planting and caring for an oak tree in a garden plot: the swamp problem has been solved

Comet NEOWIS can be seen in the July sky with the naked eye

A 2009 study from a university in Washington DC found that the heritability of depression was approximately 58% among the 1,064 pairs of female twins they studied. A similar 2006 study found that the heritability of depression was 42% in women and 29% in men. This suggests that gender also influences a person's genetic assumption.

Symptoms of endogenous depression

Endogenous depression manifests itself unexpectedly. Its signs: low mood, melancholy, anxiety, decreased self-esteem, guilt, uncertainty, increased self-criticism, hypochondria, and sometimes suicidal thoughts. Unlike the usual low mood, a depressed state is observed for a long time and cannot be corrected in the usual ways (rest, communication with friends, walks, entertainment). Patients' range of interests decreases, they become indifferent, avoid communication, and try to minimize social contacts.

The depressed psychological state of the patient may prompt him to take alcohol and other psychoactive substances.

Symptoms of endogenous depression also include mental inhibition, which consists in the inability to quickly make decisions even in an extremely responsible situation, difficulties in analyzing the information received, assessing what is happening, and concentrating; illogicality and inconsistency of thoughts and actions. The patient's movements become slower, and the rate of speech slows down. Asthenia, sleep disorders develop (insomnia, night and early awakenings), there is a decrease in appetite or excessive appetite, which is why weight is lost or gained. Dyspeptic symptoms may appear - nausea, heartburn, bad breath, constipation. Such disturbances are reflected in appearance: pale skin appears, a sallow complexion appears, hair becomes dull and brittle. Against the background of lethargy, patients may experience attacks of intense agitation, even causing harm to themselves.

The feeling of fatigue and lethargy does not leave the patient even after a long rest. Also possible are decreased libido, anorgasmia, menstrual irregularities in women, pain in the body of unknown localization, compressive pain in the heart and back pain, and a feeling of general discomfort. The depressed psychological state of the patient may prompt him to take alcohol and other psychoactive substances.

In childhood and adolescence, the prevalence of depression is 15–40%; depressive disorder in patients in this age group often leads to suicide attempts.

The patient's mood changes cyclically throughout the day. Thus, in the case of a mild course of the disease, the peak of depressed mood occurs in the morning, and by the evening the patient’s condition improves somewhat. In more severe cases, a melancholy mood and increased unreasoned anxiety are characteristic of the evening hours.

A specific sign of endogenous depression is pathological vital melancholy. At the same time, many patients can localize sensations of discomfort in a certain area of ​​the body (head, neck, chest) and differentiate this condition from pain and discomfort arising from somatic diseases, as well as from experiences formed under the influence of real causes.

There may be a feeling of unreality of what is happening (derealization), time slowing, depersonalization, a painful feeling of absence of feelings and desires, emotional perception of the surrounding reality. Patients with endogenous depression are characterized by anhedonia, which consists of a decrease or complete loss of the ability to experience pleasure. In severe cases, hallucinations occur that contain fragments of violent acts.

Nowadays, the biological mechanisms of any processes are difficult to consider without taking into account the influence of genes, and depression is no exception. Depression has a genetic component. The first thing that catches your eye; Families suffer from depression. For a long time, this would be enough for some people to see a genetic connection, but this conclusion is undermined by the obvious fact that families not only share genes, but also a common environment. When a person grows up in a poor or dysfunctional family, his risk of developing depression increases, even if he is not genetically predisposed to it.

Thus, we are looking for a closer relationship. The more closely related two people are, the more genes they share and the more likely they are to share depressive traits. As the most typical example, let's take two siblings (not identical twins). They share about 50% of their genes. If one of them had depression, the other would have about a 25% chance of getting the disease—significantly higher than the population average. Now compare two identical twins who have all the same genes. And if one of them has depression, then the other has a 50 percent chance of also getting sick. This is impressive - the more common genes, the greater the likelihood of a common disease. But there's a catch: the more genes that are shared within a family, the more similar conditions people live in (starting with the fact that genetically identical twins are raised exactly the same, unlike genetically non-identical twins).

Let's tighten the relationship even more. Consider children adopted at an early age. Take those whose biological mother suffered from depression, but their adoptive mother did not. They have an increased risk of developing depression due to the genes they share with their biological mother. But the distorting factor, as we saw in Chapter 6, is that the “environment” does not begin at birth, but much earlier - with the common circulation of the fetus in the uterus and the biological mother.

If you want to prove to any trained molecular biologist in the 21st century that genes have something to do with depression, you end up having to identify certain genes, certain stretches of DNA that encode information about the structure of specific proteins that increase the risk of developing depression. As we will soon see, this is exactly what has happened in recent years.

Immunity and depression

This subsection did not appear in previous editions of this book. Immunity is a reflection of attacks from pathogenic microorganisms, and depression is a state of sadness. At first glance, these are unrelated objects. In general, they can be connected, but in a very straightforward way, for example, illness can cause depression of the spirit.

But here the connection is more complex. A chronic illness that causes the immune system to become overactive (such as chronic infections, or an autoimmune disease where the immune system is accidentally activated and attacks some part of your body) is more likely to cause depression than other equally severe and long-lasting illnesses that do not affect the immune system. There are also lines of communication, including cytokines, which act as intermediaries between immunocytes. As you will recall from Chapter 8, cytokines can also travel to the brain, where they can stimulate CRH production. Recently it was discovered that they also interact with norepinephrine, dopamine and serotonin. It is important that cytokines can cause depression. Animal models of depression show this. Additionally, certain types of cancers are sometimes treated with cytokines (to boost the immune system), and this tends to lead to depression. Thus, the relationship between immune system functioning and mood represents a new area of ​​research for biological psychiatry.

Endocrine system and depression

Depression is often accompanied by abnormalities in the levels of many hormones. For example, people with too little thyroid hormone secretion may develop major depression and, when depressed, exhibit atypical resistance to antidepressants. This is especially important because it turns out that many people with clinical depression have thyroid disease.

There is another aspect of depression in which hormones may play a role. There are significant differences in the incidence of unipolar major depression: women suffer from it much more often than men. Even if we consider manic-depressive psychosis, the incidence of which does not differ by gender, women with this disorder experience more depressive episodes than men.

Why are women more prone to depression? This has nothing to do with the obvious first assumption that women with depression are more likely to seek treatment than men. The disparity persists even when health care visits are recorded. According to a theory based on the principles of cognitive psychotherapy, the reason stems from the fact that men and women think differently. When something out of the ordinary happens, women are more likely to reflect on the event or talk to other people. And men - far from being masters of communication - prefer to think about anything other than the problem, or, even better, do something: exercise, do some repairs, get drunk, start a war. Rumination, cognitive psychologists say, is more likely to lead to depression.

Another theory that explains differences in the incidence of depression depending on gender is psychosocial in nature. As we will see, many theories about the psychology of depression argue that the disorder stems from a lack of power and control, and some scholars have suggested that because women in many societies have traditionally had less control over the circumstances of their lives than men, they are more likely to experience depression. In support of this idea, some psychiatrists have cited data showing that elevated rates of depression in women have been reduced to levels of depression observed in men in some traditional societies in which women are not assigned a dependent role. Another theory is that men actually get depression just as often as women, but they tend to mask it with substance abuse.

All of these ideas make sense, but they fall apart when you consider that both women and men suffer from bipolar depression alike; Among women, only unipolar depression is more common. These theories seem especially untenable because they fail to explain a core feature of female depression, namely that women are especially susceptible to depression at certain times related to their reproductive function: menstruation, menopause, and most of all within a few weeks. after childbirth. Many scientists believe that the increased risk of depression is due to the large fluctuations in two major hormones, estrogen and progesterone, that occur during menstruation, menopause and childbirth. As evidence, they cite the fact that women become depressed when they artificially change the level of estrogen or progesterone in their bodies (for example, by taking birth control pills). It is very important that both of these hormones can regulate neurochemical processes in the brain, including the metabolism of neurotransmitters such as norepinephrine and serotonin. It is now thought that when there are huge fluctuations in hormone levels (for example, during childbirth there can be a thousand-fold change in progesterone levels), the estrogen to progesterone ratio may change enough to cause major depression. This is a new area of ​​research, and there are already some conflicting results, but there is growing confidence among scientists that the predominant incidence of depression among women is to some extent explained by hormones.

Obviously, glucocorticoids will be the next object of study on the relationship between hormones and depression. But given how important this is to the theme of our book, the subject requires detailed consideration.

Stress, glucocorticoids and the onset of depression

The main connection between stress and depression is obvious and is that stress is usually accompanied by depression. This connection can develop in two ways. First, studies of what is called “stress generation” among depressed patients show that people prone to depression can experience stress even in places where they are not expected. This is noticeable even when comparing such people with people with other mental disorders or physical illnesses. Much of this stress appears to result from a lack of social support. As a result, a vicious circle is likely to form. The mechanism is this: if you interpret ambiguous social interactions around you as signs of a negative attitude and react accordingly, then you tend to distance yourself from people and thus become convinced that they treat you poorly...

But in general, the causal relationship we are interested in between stress and depression follows a different path. In particular, people who experience a lot of stress in their lives are more likely than average to experience major depression, and people who are newly depressed tend to be more likely to experience major stress. Of course, not everyone who is exposed to severe stress becomes deeply depressed, and we will explore the differences between such people later in this chapter.

As I said, some people are very unlucky to suffer from recurring episodes of depression, which can become periodic in a cycle lasting several years. Looking at the medical histories of such people, we see that stress factors act as triggers only for the first few depressions. In other words, once you experience two or three bouts of major depression, you are statistically more likely to become deeply depressed again in the future than anyone else. But somewhere around the fourth depression or so, this crazy mechanism starts up on its own, and waves of depression roll over you regardless of whether the outside world gives a reason for this. What causes this change will be discussed below.

Laboratory studies have also found a link between stress and depressive symptoms. Put a lab rat under stress and it will lose its ability to experience pleasure in life. In particular, it would take a stronger electrical shock to produce a feeling of pleasure in a rat's brain. The threshold for the perception of pleasure is elevated, just like in a depressed person.

Crucially, glucocorticoids can do the same. The key point in Chapter 10 was that glucocorticoids and stress can destroy memory. Part of the evidence for this came from people with Cushing's syndrome (a condition in which certain types of tumors cause too much glucocorticoids in the blood), as well as people who were prescribed large doses of glucocorticoids to treat certain diseases. It has long been known that many patients with Cushing's syndrome and patients prescribed synthetic glucocorticoids become clinically depressed regardless of memory problems. It was quite difficult to prove this. First, when a person first begins to be treated with synthetic glucocorticoids, he tends - if he does at all - to become euphoric or even overexcited for about a week before depression sets in. One can immediately assume that we are dealing with one of our dichotomies between short-term and long-term stress: Chapter 16 explores in more detail where this transitional period of euphoria comes from. Another difficulty is the need to decide whether a person with Cushing's syndrome or someone taking high doses of synthetic glucocorticoids becomes depressed because the glucocorticoids cause the condition, or whether it occurs as a result of the person's awareness that he has depression. You argue that glucocorticoids are to blame because depression is more common among people who take them than among people who suffer from the same illness and the same severity but do not take glucocorticoids. At this stage, the mechanism for scientific forecasting of this phenomenon is not sufficiently developed. For example, no clinician can predict with certainty which patient will become depressed after high doses of glucocorticoids—let alone what dose will be required—and whether this will happen when the dose is increased or decreased to that level. However, if you have high levels of glucocorticoids in your blood, your risk of depression increases.

Regarding a person's susceptibility to depression, there is another important contradiction between stress, glucocorticoids and the biological mechanism of this disease. Let's return to the question that there is a genetic component to depression. Does this mean that if you have the “depression gene(s)”—that is, you are susceptible to the disease—then you will definitely suffer from it? Of course not, and the best proof of this is the speculative assumption of identical twins. One of them has depression, and the other, who has the same genes, has a 50 percent chance of also getting the disease—significantly higher than the population average. Here's some pretty compelling evidence that genes also play an important role in the development of depression. But let's look at this from a different angle. If you have every single gene the same as someone who has depression, you still have a 50 percent chance of not getting the disease. Genes rarely indicate inevitability, especially when it comes to people, brains or behavior.

Genes indicate vulnerability, susceptibility, propensity. In this case, the genes increase the risk of depression only in certain environments—you guessed it—only stressful environments. This has already been proven in many ways, but most impressively by a recent study by Avshalom Kaspi of King's College London. Scientists have found a certain gene in people that increases the likelihood of developing depression. More specifically, it is a gene that has several “allelic versions”—several different types that have slightly different functions; if you have one of these versions, you are at risk. I'll save the story about this gene for the end of the chapter, because it's something mind-blowing. But the main point is that having version X of that gene Z does not guarantee that you will get depression, it only increases your risk. And in fact, even if you only know about a person what version of the Z gene he has, this will not allow you to say with certainty that he has depression. Version X only increases the risk of depression when a person has already had several bouts of major depression. Surprisingly, the same thing was shown by studies on some species of monkeys that have a close equivalent of the Z gene. Let me emphasize that it is not the gene that causes depression. Depression occurs due to certain circumstances. That is, the gene makes you vulnerable in a stressful situation.

Glucocorticoid profiles after diagnosis of depression

It is not surprising that people with clinical depression exhibit abnormalities in glucocorticoid levels. In a relatively uncommon subtype of depression, called atypical depression, the dominant psychomotor symptom is disabling physical and psychological exhaustion. As with chronic fatigue syndrome, atypical depression is characterized by extremely low levels of glucocorticoids. However, a much more characteristic feature of depression is an increased response to stress—an overactive sympathetic nervous system and even higher levels of glucocorticoids. This adds color to the overall picture of depression, when a person sits on the edge of the bed, not having the strength to get out of it; at the same time, he is alert and excited, and his hormonal profile is appropriate - but only the battle takes place inside him.

About 40 years ago, scientists found that in depression, glucocorticoid levels increase due to too many stress signals coming from the brain (in Chapter 2 we said that the adrenal glands, as a rule, produce glucocorticoids only when appropriate stress comes to them through the pituitary gland). command from the brain), and not because they themselves produce them in increased quantities from time to time. Additionally, excess glucocorticoid secretion occurs due to what is called a feedback level—in other words, the brain is not as effective as it should be in stopping the production of glucocorticoids. Typically, the levels of these hormones are tightly regulated - the brain senses the level of glucocorticoids in the blood, and if it becomes higher than the desired level (the "desirable" level fluctuates depending on whether stress is caused by events), the brain stops secreting CRH. Just like adjusting the water level in a toilet tank. In people with depression, feedback regulation is impaired—the body cannot reduce the concentration of glucocorticoids in the blood because the brain does not sense the feedback signal¹. What are the consequences of elevated glucocorticoid levels before and during depression?

The first and most important question to ask is: How much does elevated glucocorticoid levels increase the likelihood of depression?

________________________________________________

¹ Attentive readers will remember what was discussed on p. 248 dexamethasone suppression test, showing that the body of older people may have difficulty stopping the production of glucocorticoids. The same test is used here. And the careful reader will recall that in aging, the problem of glucocorticoid production stopping—“dexamethasone resistance”—is likely the result of damage to the part of the brain that helps stop the stress response when increased amounts of glucocorticoids are produced. Does similar damage occur in depression? As we will see, this happens in some people who have been depressed for a long time. However, elevated levels of glucocorticoids occur in people with depression even if their brain is not damaged. Most likely, prolonged stress reduces the number of glucocorticoid receptors in this part of the brain, making neurons less sensitive to the level of this hormone in the blood.

The previous section detailed much confusion regarding whether serotonin, norepinephrine, or dopamine contribute to depression. The fact is that hormones can change the properties of all three neurotransmitter systems - the number of neurotransmitters synthesized, the rate of their breakdown, the number of receptors corresponding to each neurotransmitter, the quality of the receptors, etc. In addition, it turned out that stress also causes many of these changes . Prolonged stress flushes dopamine from the “pleasure center” and norepinephrine from the “blue spot” of the brain, which puts the body in a state of readiness. Stress also changes all aspects of serotonin synthesis, secretion, efficiency, and breakdown. It is unclear which of these stress effects are most important, simply because it is unclear which neurotransmitter(s) are most important. However, we can say with confidence that no matter what neurochemical abnormalities trigger the mechanism of depression, stress and glucocorticoids cause the same abnormalities.

Elevated levels of glucocorticoids also have other consequences. For example, partly for this reason, people with depression often have lower immunity and are more prone to osteoporosis. In addition, long-term major depression increases the risk of heart disease by approximately three to four times, even if the patient does not smoke or drink alcohol; this is also likely facilitated by excess glucocorticoids.

There could be even more consequences. Recall that in Chapter 10 we discussed the many ways in which glucocorticoids can harm the hippocampus. The literature on this topic, which appeared in the 1980s, quickly began to suggest that people with major depression may have problems with the hippocampus. This assumption was supported by the fact that the type of memory most often affected in depression—declarative memory—is regulated by the hippocampus. Chapter 10 stated that long-term depression causes atrophy of the hippocampus. Atrophy is a result of depression (not a precursor to it), and the longer depression lasts, the greater the atrophy and the more memory problems. Although no one has yet proven definitively that atrophy occurs only in depressed people who have elevated glucocorticoid levels, it is most common in subtypes of depression that are characterized by excess glucocorticoids. Chronic depression has also been linked to reduced frontal cortex volume in some studies. Those of us who look at the world through the lens of glucocorticoid content were initially puzzled by this statement, but the issue has recently become clearer. In the rat, glucocorticoids act only in the hippocampus. It turns out that there is the highest density of receptors for these hormones. And in the primate brain, the hippocampus and frontal cortex are equally and markedly sensitive to glucocorticoids.

Thus, there is fairly strong circumstantial evidence that excess glucocorticoids in depression may have something to do with reduced hippocampal and frontal cortical volume.

Chapter 10 covered the many nasty things glucocorticoids can do to neurons. Some very careful studies have shown that in depression, the frontal cortex loses cells and shrinks in volume - adding to the uncertainty is the fact that it is not neurons that are lost, but supporting glial cells. But as far as the hippocampus is concerned, the situation is unclear; this could be neuronal atrophy, an obstacle to the formation of new neurons, or all of the above¹. Whatever the explanation for this volume loss at the cellular level, it is permanent, persisting years and even decades after clinical depression is brought under control (usually with medication).

_________________________________________________________

¹ Chapter 10 details the revolutionary discovery that the adult brain, specifically the hippocampus, can create new neurons. It also turned out that stress and glucocorticoids are the most powerful inhibitors of this process. It also noted that it is not yet clear what these new neurons are for, although it would be reasonable to assume that the new neurons in the hippocampus would be good for memory. Thus, it can also be assumed that inhibition of the formation of new neurons in the hippocampus before and during depression may play a role in the occurrence of the memory problems already discussed. This seems convincing to me. But another idea is that inhibiting the formation of new neurons also contributes to emotional symptoms (that is, the complete indifference to the pleasures of life and the sadness that define depression) and that antidepressants trigger the process of the formation of new neurons in the hippocampus. This theory has received a lot of attention and there have been many solid studies done to prove its validity. However, I find these studies and the underlying message not very convincing—I can find links between hippocampal function and emotional disturbances in depression, but they will seem too complex to be called the main cause of this disease. (You may have noticed that I included this comment in a footnote in the hope that some of my colleagues whom I like and respect but who hold the opposite opinion will not come to me to bash me.)

Previous – Biological mechanism of depression | Next – Antiglucocorticoids as antidepressants

Diagnostics

The diagnosis of endogenous depression is established on the basis of the patient’s complaints, medical history, as well as assessment of the level of depression using special tests (Zang scale for self-assessment of anxiety, Beck depression scale, test for determining the level of depression, adapted by T. I. Balashova, etc.).

An important indicator for diagnosing endogenous depression is the patient’s pronounced mental retardation (slowing down the rate of speech, speed of thinking, patients need more time than usual to express their thoughts and formulate answers to the questions posed). A slowdown in the rate of speech is noted throughout the entire dialogue with the patient, which distinguishes endogenous depression from asthenic conditions.

Endogenous depression occurs for no apparent reason (not associated with psychogenic or situational exogenous factors).

If endogenous depression is suspected, a laboratory examination is carried out, including determination of the level of hormones in the blood, hemoglobin content, etc. If there are signs of somatic pathology, the patient is referred for consultation to specialists (endocrinologist, gastroenterologist, etc.).

Endogenous depression must be differentiated from psychogenic depressive disorder, which is characterized by a connection with obvious or hidden psychological trauma.

Diagnosis and treatment of depression

Diagnostics is performed in a specialized medical institution by a psychiatrist. To make a diagnosis, additional information may be required, in particular, interviewing people who are in regular contact with the patient. The disease is treated with drug therapy. Antidepressants for endogenous depression and other groups of drugs are prescribed individually, depending on the course of the disease.

In modern psychiatry, complex treatment methods are very popular. In addition to antidepressants, the patient must regularly take mood stabilizers. This group of medications can improve the patient’s mood and prevent the development of secondary symptoms.

Before starting treatment, the specialist must identify the cause of depression. The work of psychologists with the patient during the treatment process will improve the patient’s personal assessment and identify the cause of the disorder.

Recovery does not happen immediately. In the first few weeks after starting antidepressants, there is a gradual decrease in depression and anxiety. Mental retardation subsides 16-20 days after starting medication. Suicide attempts, delusional ideas and hallucinations can persist for 4-5 weeks.

Antidepressants are taken throughout the entire treatment course. Stopping treatment on your own will worsen the patient's condition.

Treatment of endogenous depression

Treatment of endogenous depression is usually carried out in an outpatient setting. In severe cases, hospitalization may be indicated. It is necessary to eliminate possible factors that stimulate the development of pathology, which requires correction of the patient’s lifestyle, including normalization of work and rest, nutrition, etc.

The main method of treating endogenous depression is the use of antidepressants, which should be continued for some time after the symptoms of the disease have completely disappeared, since if therapy is stopped prematurely, there is a risk of deterioration of the patient’s condition and relapse. In addition, abruptly stopping antidepressants may cause withdrawal symptoms. As a rule, motor and mental retardation decreases after 2-3 weeks of drug treatment, but depressed mood and suicidal thoughts may persist somewhat longer.

In addition to antidepressants, mood stabilizers can be used to help stabilize mood and prevent the development of new episodes of depression.

Patients' range of interests decreases, they become indifferent, avoid communication, and try to minimize social contacts.

Psychotherapy plays a supporting role in the treatment of endogenous depression, serving as a complement to drug therapy. The most common methods of psychotherapy for depressive disorders are:

• existential – aimed at realizing one’s life values;
• cognitive-behavioral – aimed at increasing activity, acquiring social competence, training self-control, reducing the severity of the patient’s negative ideas about himself and the world around him, eliminating residual symptoms after successful drug therapy;
• interpersonal – teaching social skills that caused difficulties for the patient;
• psychodynamic – based on the theory of psychoanalysis;
• client-centered ; etc.

Source: ufavesti.ru

A set of physical exercises is prescribed due to the impact of physical activity on the neurotransmission of certain mediators (increased production of serotonin, β-endorphins), increased body temperature and, accordingly, metabolic rate, increased body tone. Patients are recommended to practice yoga, take vitamin and mineral complexes, and take long walks in the fresh air.

Ancillary methods for treating endogenous depression include phototherapy, sleep deprivation, low-frequency alternating magnetic field therapy, vagus nerve stimulation, massage, art therapy, occupational therapy, and aromatherapy.