Anti Depressants are entering the everyday life. And despite the fact that there is a consensus in the professional community about their effectiveness in the treatment of depression, the use of antidepressants in society is not considered something healthy. Many of those who take these drugs in the hope of improving their mental state are confronted with misunderstandings from relatives and friends, who often consider their reception a whim or even the result of a conspiracy of pharmaceutical companies. The Village asked the scientific journalist Svetlana Yastrebova to explain how antidepressants actually work, whether to fear their spread and why myths about inefficiencies are born around them.
Since the early 2000s, the frequency of Anti Depressants use has increased in almost all countries. In 2000, most of these drugs were used by residents of Iceland: 71 people out of a thousand admitted that they regularly use them, and in 2011 this number increased to 106 people per thousand. In Canada and Australia, the figures are not much better: in 2011, 86 and 89 out of a thousand people resorted to medication against depression, respectively. Scandinavians and other Europeans lagged, but not much. Residents of the countries of Eastern Europe avoid the constant intake of antidepressants, but they often use them once (to be honest, it does not make much sense for health). Women treat depression more often than men, and bisexuals are more likely to be homosexual and heterosexual. In Russia, alas, there is no exact data.
Chemistry of the process
Unequivocally correct answer to the question “what causes depression” is not, and it is unlikely he will soon appear. There are several theories of depression, and most of them are somehow tied to neurotransmitters – substances that transmit a signal from one nerve cell to other nervous or muscle cells. The most popular hypothesis is serotonin. It states that in patients with depression, the production of serotonin itself, or its perception, is disrupted. Most medications against depression are designed to eliminate this problem. One of the newest and most frequently used is selective serotonin reuptake inhibitors (SSRIs). They trap the molecules of serotonin in the gap between the two nerve cells, as a result of which the effect of the neurotransmitter appears longer and stronger. The work of other neurotransmitters SSRIs should not act.
Means of previous generations have more side effects. This, for example, inhibitors monoaminoksidazy (MAO) – an enzyme that destroys serotonin and dopamine. Since these two neurotransmitters act not only on the mood, but also on many other processes in the body (for example, serotonin enhances intestinal motility, and also narrows vessels, which to some extent controls the erection), MAO inhibitors can produce a wide variety of side effects. Therefore, they are used much less often than SSRIs, and even if possible in the clinic, under the constant supervision of a physician.
There is another opinion as to the causes of depression. It is known that with depression almost no new bonds are formed between nerve cells. This is probably the cause of the disease. Perhaps, serotonin does not affect the mood at all, but only helps to launch an enhanced formation of contacts between neurons. If this is the case, it becomes clear why most antidepressants raise their mood not immediately after the first reception (like food and alcohol), but only after two weeks, and why SSRIs sometimes help with anxiety disorders that are not specifically associated with serotonin.
Why not choose Anti Depressants yourself?
First, you do not know what causes depression specifically in your case. Chemistry of the process as a whole is not known to the end, and even more so to determine by eye, which system of neurotransmitters has broken down specifically in your case, will not work. In addition, there are many clinical studies and their meta-analyzes that show: antidepressants help only if the severity of the disease is above average. Most likely, a person who is actually able to help with antidepressants, feels so bad that he can not think of any choice of tablets himself.
The severity of depression psychiatrists define in several ways. One of them is the so-called Hamilton scale. Most often it is used in the study of the effectiveness of individual drugs. It includes 21 questions about the patient’s condition. Each answer gives a certain number of points, and the more they are total, the heavier the depression. The maximum possible number of points is 23, the mild depression starts from 8, the heavy one starts from 19. The medication is considered effective if due to it the patient’s account on the Hamilton scale falls at least three points lower than from the “treatment” with the help of a placebo. Such a fall does not occur in patients with mild and moderate depression.
And finally, like any substance that interferes with brain chemistry, any antidepressant has a wide variety of side effects – from constipation and erection problems to the realized desire to die. Of course, the safest drugs out of the possible come to the pharmaceutical market, and their direct and side effects are investigated in animals and in the clinic. Along with this, no one canceled the so-called publication bias: both in medicine and in basic science, positive results of research are published more often, and the undesirable ones are silent. That is, no one is lying, but some people are not telling the truth. In part, this is due to the demands of organizations for controlling drugs to antidepressant manufacturers. For example, the Office of Food and Drug Administration (FDA) in its documents takes into account only those side effects that were observed during the study itself and within a day after its completion. If anything happens to a participant in the study after this period, it will not be recorded anywhere.
Are there ways to quickly find the right medicine?
Studies of new antidepressants, in which hundreds of volunteers are involved, is, of course, good. Only they do not abolish the fact that each specific person has a long and sometimes painful choice of a drug that will suit him. This is a sad fact, but it can not be avoided, although various pharmaceutical companies periodically offer miraculous ways of predicting the actions of an antidepressant on a particular person. For example, there have been repeated attempts to understand whether the tablet will act, according to how the patient’s electroencephalogram changes – the frequency and strength of the waves of electrical signals that the cells of his brain send.
The results of research on this topic were initially encouraging, but on closer examination, noticeable flaws were found in the course of the experiment. For example, in one of the works there were two groups of patients – those who were constantly given the same antidepressants, and those who could change the drug, if EEG patients “showed” that it needed to be done. In people from the latter group, the severity of depression fell faster and lower. That’s just the fact that these people were initially treated with other pills, not like the members of the first group. So the effectiveness of therapy here can not be compared at all.
The authors of the other two papers did not make such a stupid mistake, and it all turned out that their method of predicting the effectiveness of EEG antidepressants works. But this if you do not look at the formula for translating EEG readings. Half of the variables in it have meanings unknown to anyone other than the authors of the articles. And the authors did not consider it necessary to share this information with the rest.
Choosing the right antidepressants for genes, to be honest, does not work either. In the article, which describes the selection algorithm itself, it is described that 51 subjects with depression were divided into two groups. One genomic algorithm of the company AssureRx “advised” specific antidepressants, and another drug was selected by a psychiatrist. At first the treatment was equally successful in both groups, and after eight weeks the condition of the patients who listened to the psychiatrist, for some reason, deteriorated sharply. Here it must be taken into account that all participants in the study knew who had given them the medicine, a psychiatrist or a geneticist. So the users of the AssureRx algorithm could just really want them to get better faster, and the placebo effect really helped them. In addition to everything in the original article does not say what the tablets were taken by the subjects. Maybe they each had their own.
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