Is depression directly related to genetic factors?

  Research on depression is very active, not only because of the large number of people who suffer from this disorder, but also because it is a drug market with great potential. Unfortunately, as with most other psychological disorders, research on the mechanisms of depression is still very immature and many basic questions remain unanswered.  But one thing is certain: it is a genetically related disorder. One study showed that children born to parents who had depression were significantly more likely to have depressed children than normal parents. In order to distinguish between genetic factors and the influence of the acquired environment, researchers also counted the children of depressed parents who were adopted by normal parents, and the results still proved that the adopted children were more likely to have the disease than the children of normal parents. Another study on twins appears to be more convincing. If one of the identical twins suffered from depression, the other became more likely to have the disease than the heterozygous twin.  Whether or not depression is a genetic disorder has a significant impact on the choice of treatment. If it is, it means that depression is related to the structure of the human brain or some kind of chemical reaction, which can be treated by chemical drugs. Otherwise, if depression is just a psychological disorder, one should see a psychiatrist.  In fact, for the first 50 years of the last century, psychology was ruled by Freudian psychoanalysis, and psychotherapy was the only option for psychiatric patients. . This was the first chemical drug to treat schizophrenia.  In order to reduce the side effects of chlorpromazine, scientists continued to fine-tune the molecular structure of chlorpromazine and then experimented on the newly created chemical molecules in humans. Unexpectedly, one of the small molecules, code-named G22355, had the opposite effect of chlorpromazine, making the user hyperactive for no reason. Later, this small molecule, named “Mipramine”, became the first drug to treat depression.  The discovery of another antidepressant, isonicotinyl isopropyl callus, is even more legendary. “The German army invented a rocket fuel, hydrazine, during World War II, and after the war was over, it was useless and was used by chemists for drug testing. Their intention was to find a cure for tuberculosis, but instead they discovered that a variant of hydrazine, isonicotinylisopropylhydrazine, could give subjects an inexplicable high. Thus, a second drug for depression was invented.  In the 1980s, similar drug screening led to the selection of a new class of antidepressants, the “selective serotonin reuptake inhibitors” (SSRIs), of which the famous “Prozac” was an SSRI. Prozac had the fewest side effects of any known antidepressant at the time, so it quickly became popular worldwide and really became a veritable “people’s sorrow reliever”.  It is worth mentioning that the mechanism of action of these drugs was not understood until many years after they were marketed. Chlorpromazine is a dopamine antagonist, isoniazid is a monoamine oxidase inhibitor, mipramine is a pentraxin receptor inhibitor, and Prozac is, as the name implies, an inhibitor of the serotonin reuptake process.  In essence, all of these drugs act on small molecule messengers in the brain that transmit information, scientifically called “neurotransmitters. Among them, pentraxin and serotonin are actually two names for a neurotransmitter, a compound that is associated with affective disorders and is widely believed to be a key factor in depression. According to research, serotonin levels in the brains of depressed patients are lower than in normals, so the main effect of antidepressants is to increase serotonin levels, or the efficiency of serotonin receptors.  This theory has been validated by genetics. The gene most likely to cause depression is known to be called 5-HTT, which encodes a protein responsible for transporting serotonin. There are two types of this gene, one long and one short. A human experiment conducted over a two-year period showed that a person with two copies of the long type 5-HTT gene had a 17 percent chance of feeling depressed when under stress. If the person had one long and one short copy, the likelihood increased to 33%. If he was unfortunate enough to have both copies of the short type, then the likelihood of having the disease increased to 43%. This experiment shows that the short 5-HTT gene is not sufficient to cause depression, but it can reduce the person’s self-control when dealing with a crisis.  So, is increasing serotonin levels a cure for depression? It is far from simple. As you can see from the above account, almost all drugs for psychiatric disorders are discovered by accident, not designed by scientists, because human research on the brain is still in its infancy and many issues are not fully understood. Serotonin, for example, has a wide range of effects, and boosting its levels indiscriminately is likely to cause some unexpected side effects.  Even the relationship between serotonin and depression has been questioned. A number of independent agencies have issued warnings to be wary of the results achieved by scientific research funded by pharmaceutical companies. This confusion between money and science is most evident in the field of depression research, because it is a difficult disease to define, everyone is occasionally depressed for a while, to what extent should you take medication? Sometimes even the experts can’t say.  Pharmaceutical companies, of course, want people to take drugs. Henry Gadsden, the former CEO of Merck, once criticized the company’s approach as “limited to the patient. He meant that pharmaceutical companies should find ways to sell drugs to healthy people, only then can get the most profit.  As a result, many people accused the pharmaceutical companies of buying scientists and spreading false information to persuade people who could have been cured through psychotherapy to enter the pharmacy. But others point out that some of the critics themselves are involved with psychotherapists or those “alternative clinics. Neither side of the argument is clean.  Until the mechanism of any disease is completely understood, it will certainly look like this, and this is especially true of depression. How should it be treated? It’s a depressingly complex question.