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Antidepresanlar Çalışıyor mu? — Transcript

by Evrim Ağacı · 4,390 words · 781 segments · language en · Watch on YouTube

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0:00How are you feeling mentally right now?
0:02Do you feel peaceful, happy, and
0:04satisfied with your life?
0:07Or do you feel restless, tense, and
0:09chronically stressed?
0:12I ask this because one of the most
0:14dangerous consequences of chronic stress
0:17is that it leads to depression, and
0:19statistics tell us that one in every 10
0:21to 20 individuals over the age of 18
0:23watching this video is currently
0:25depressed, and I suspect a significant
0:27portion of these people are also taking
0:29antidepressants regularly.
0:32Because statistics indicate that in
0:35Turkey, one in every 10 people may be
0:37taking antidepressants.
0:40I don't know the exact numbers for
0:42Turkey, but in the United States alone,
0:44more than 100 million prescriptions were
0:46written for three different types of
0:48antidepressants in 2024.
0:51Think about that. 100 million. So, do
0:54these drugs actually work? I mean, when
0:57you take these medications, do you feel
0:59your depression subsiding?
1:01Or are you among those who have tried
1:03these drugs and didn't see any benefit?
1:06Do we really know how antidepressants
1:10work?
1:11Let's take a look.
1:14Before we move on to the video, I have a
1:16small announcement. We are currently
1:18developing the Evrim Ağacı Android and
1:20iOS apps at a truly incredible speed.
1:24For instance, we have chat rooms where
1:26you can chat live with other science
1:28enthusiasts instead of using Discord,
1:30and currently, more than 10,000 people
1:32are members of these rooms, or we are
1:34developing truly enjoyable science games
1:37for you.
1:39You can also play them for free on our
1:41app.
1:42I am leaving the links below. Definitely
1:44download our app and turn on
1:45notifications.
1:47We are building a very serious community
1:49of science lovers there. We would love
1:50to see you there too. Now,
1:52antidepressants.
1:56Depression is an extremely insidious and
1:59cruel mental illness that causes people
2:02to feel sad and empty and to lose
2:04interest in life.
2:07Of course, we call them all depression,
2:08but there isn't actually just one
2:10clinical picture of depression.
2:12There are many types, such as major
2:15depressive disorder, depression
2:17accompanying bipolar disorder, prenatal
2:19or postpartum depression, and psychotic
2:22depression; and behind each of these
2:24different types of depression lie
2:26biological factors like brain chemistry
2:28, brain structure, family history, and
2:31genetics; psychological factors such as
2:33personality traits, the ability to cope
2:36with difficulties, or post-traumatic
2:38stress disorder;
2:41and social and environmental factors
2:43like substance abuse or traumatic and
2:45stressful life events.
2:47But this video is not about depression.
2:50Today, we will focus on antidepressants
2:52.
2:54But for those who are curious, I'm
2:56leaving a few of our articles on
2:57depression below, and if you would like
2:59to see a video about depression, you can
3:01send it to me directly via the video
3:03section in the mobile app I just
3:05mentioned.
3:07Because depression itself is the subject
3:09of another video.
3:11Now, let me say this right from the
3:12start.
3:13We do not know how antidepressants work
3:15.
3:16Yes.
3:18Even though they are prescribed to
3:20hundreds of millions of people every
3:21year, we have not yet fully deciphered
3:23which of the changes they create in our
3:25bodies is the one that affects us.
3:29I know this sounds terrible, but
3:30actually, this is not considered very
3:32abnormal for medicine.
3:34For example, we still do not know
3:36exactly how the most common anesthetic
3:38agents used in surgeries work.
3:40In fact, never mind these sophisticated
3:42drugs. We still haven't fully solved how
3:45an ordinary painkiller like paracetamol
3:47—which I mentioned to you before in the
3:50context of autism and which you know as
3:53Parol—actually works. And these are used
3:55much, much more widely in modern
3:57medicine than antidepressants. I will
4:00get to why we don't yet know how these
4:03common drugs work in just a moment.
4:06But first, how can it be that we don't
4:11know how these drugs, which are just
4:16chemical substances, function?
4:21Just like water, air, or the food we eat
4:24. And like every chemical substance,
4:27when drugs enter our bodies, they cause
4:30various changes by binding to other
4:33molecules, altering them, or reacting
4:35with them to create new products.
4:39Since we are all members of the same
4:41species, and more importantly, since
4:44more than 99%of our DNA is exactly the
4:47same, the changes a chemical creates in
4:49our bodies are generally more or less
4:52the same.
4:54Therefore, when we take 100 people with
4:57similar characteristics, give a drug to
5:0050 of them, and withhold it from the
5:02other 50, we can generally understand
5:05the drug's effects on our species by
5:07looking at the changes in the biology,
5:10psychology, and physiology of these two
5:13groups after a certain period.
5:16This is essentially what we call a
5:18controlled experiment in science.
5:21And even if controlled experiments
5:23cannot show the exact mechanism by which
5:26a drug acts, they allow us to understand
5:28whether that drug has any effect and, if
5:31so, to what extent.
5:34That is why we can use drugs on a large
5:36scale and get results from them even if
5:38we don't fully know their mechanisms.
5:42This is exactly why your headache goes
5:44away almost every time you take
5:45paracetamol when you have a headache.
5:49Or this is exactly why the anesthetic
5:50agent is able to put you to sleep every
5:52time you lie on the operating table, no
5:54matter what you do.
5:56We are not sure about their mechanisms,
5:58but we are sure that they work. And this
6:01is not actually something unique to
6:03medicine. For example, in physics, we
6:05don't know how wave function collapse or
6:08entanglement works, but we know their
6:10effects very well. Therefore, we can use
6:13them in our engineering.
6:15So much so that the motto of the
6:16classical interpretation of quantum
6:18mechanics, which I told you about before
6:19, is "shut up and calculate."
6:21In other words, don't get hung up on
6:23whether it's the parallel universe
6:24interpretation of quantum or the Bohmian
6:26interpretation. Just do your calculation
6:28and move on. They say what matters is
6:30that the calculation works. Anyway. Of
6:32course, the fact that we don't fully
6:35know a drug's mechanism doesn't mean we
6:37don't know anything about it.
6:40For instance, we know that Parol can
6:42reduce the activity of cyclooxygenase
6:44enzymes and the production of
6:46prostaglandin.
6:47And it is thought that these effects
6:49contribute to the relief of pain. But
6:52the p-aminophenol, which can be formed
6:54by the breakdown of the same molecule in
6:57our liver, can combine with arachidonic
7:00acid in our nervous system via an enzyme
7:02called fatty acid amide hydrolase to
7:05transform into another chemical called
7:07AM404.
7:09This molecule might also suppress pain
7:11transmission by stimulating TRPV1
7:13receptors and indirectly strengthening
7:16cannabinoid signaling, or perhaps
7:18paracetamol itself activates
7:20serotonergic pathways to provide an
7:22increase in serotonin, thereby
7:24suppressing our sense of pain.
7:28You don't need to understand what these
7:30technical terms mean, but I can convey
7:32them to you this clearly because we know
7:34each of these different mechanisms
7:36inside and out very well.
7:39The problem is that we don't know which
7:41of these mechanisms is the primary one,
7:43whether several are working
7:45simultaneously, or if there is another
7:47mechanism involved that we have yet to
7:49discover.
7:50But we are sure that the drug somehow
7:52stops the pain. And we also know that
7:55this path is not through magic or
7:57sorcery. Therefore, research is ongoing
8:00.
8:01Another issue regarding these types of
8:03drugs is the matter of our DNA being 99
8:05%the same, which I just mentioned.
8:08This is actually completely true, but as
8:10we always talk about on this channel,
8:12biology is not a branch of science like
8:13physics.
8:15It is incredibly chaotic.
8:17In other words, changes in those 30
8:19million nucleotides—which is 1%of the 3
8:21billion nucleotides found in every cell
8:24in our body—when combined with the
8:26complex networks genes form with each
8:28other or with gene-environment
8:29interactions, can cause an individual to
8:32have a completely different physiology,
8:34anatomy, or psychology even from their
8:36own sibling.
8:38This can fundamentally change the effect
8:40that the exact same drug creates in the
8:42body.
8:44Therefore, a drug that works for one
8:45person might not create the same effect
8:47in another.
8:49Now let's come to antidepressants.
8:52Everything I've explained so far applies
8:54exactly to antidepressants as well.
8:57Look, until the 1950s, attempts were
8:59made to cure depression using methods
9:01like psychotherapy, developed by Sigmund
9:04Freud and his followers, and
9:06electroconvulsive therapy, which
9:07stimulates the brain electrically.
9:11The start of treating depression with
9:13medication actually arose from two
9:15completely unrelated medical
9:16coincidences.
9:19In 1952, during trials for a drug called
9:21iproniazid, originally developed for
9:23tuberculosis, an unexpected improvement
9:26in the mood of depressed patients taking
9:28the drug was noticed.
9:31Just 4 years after this discovery, the
9:33Swiss psychiatrist Roland Kuhn observed
9:35that a molecule called imipramine—which
9:38was actually being tested for allergic
9:40reactions and developed in the hope that
9:42it might have antipsychotic effects—
9:44created a revitalization in patients
9:46with depression.
9:49So, for the first time until that day,
9:50it was seen that a chemical administered
9:52to the body was good for an abstract
9:54disease like depression.
9:56In that case, there must have been brain
9:58chemistry behind depression. Don't you
10:00think? These two coincidences opened a
10:02brand new door in the history of
10:04neuroscience.
10:06Researchers discovered that these drugs
10:08affect neurotransmitters in the brain,
10:10such as serotonin and noradrenaline.
10:13As you know, neurotransmitters are small
10:15molecules that provide transmission
10:17between the connections called synapses
10:18that our brain cells make with each
10:20other.
10:21Following this discovery, years went by
10:24. That iproniazid and its derivatives
10:27turned into monoamine oxidase inhibitors
10:29, which prevent the breakdown of these
10:31chemicals I call neurotransmitters, and
10:33the other drug I mentioned, imipramine,
10:36turned into tricyclic antidepressants,
10:38which prevent these molecules from being
10:40reabsorbed from the synaptic cleft. As
10:42these drugs developed, what we didn't
10:45know about them started to increase as
10:47well.
10:48For example, the level of therapeutic
10:50power of tricyclic drugs like
10:52amitriptyline in severe melancholic
10:53depression has still not been fully
10:55understood to this day.
10:58But thanks to stable and persistent
11:00experiments, we managed to reinforce
11:02these drugs from different angles.
11:04For instance, these first-generation
11:06drugs I've mentioned so far worked
11:08literally like a shotgun in the brain.
11:11That is, they affect a very wide network
11:12of receptors.
11:14Due to their anticholinergic properties
11:16, they caused side effects like dry
11:18mouth and constipation, and they could
11:19affect heart rhythm.
11:22Consequently, severe headaches,
11:24dizziness, cognitive clouding, and, most
11:26importantly, fatal dangers in the event
11:29of an overdose could emerge.
11:31So, science needed a more sniper-like
11:34weapon.
11:36By the 1970s, scientists began to lean
11:38toward the idea that increasing
11:40serotonin transmission in our brain
11:42cells in a more selective manner could
11:44treat depression.
11:47This more narrowed-down, or rather, more
11:50sniper-like target gave birth to the
11:52first selective serotonin reuptake
11:54inhibitors, or by their famous name,
11:57SSRI-type drugs, in 1988.
11:59The name of that first drug was
12:01fluoxetine, or by its more famous name,
12:04Prozac.
12:05Prozac created a real revolution in
12:07antidepressants, but its greater success
12:10was triggering a cultural shift.
12:13Because back then, just as some people
12:16today mistakenly believe that obesity is
12:18caused by a lack of willpower or a lack
12:21of self-control, people at that time
12:23believed that the main cause of
12:25depression was such personal
12:27inadequacies.
12:30But as science showed that depression
12:32was an independent biological disease
12:34rather than a matter of individual
12:35choice, it began to break the
12:37stereotypical beliefs held by society
12:39about depression.
12:41Following this, throughout the 1990s,
12:43while the use of antidepressant drugs
12:45climbed rapidly, treatments like
12:47psychotherapy were increasingly pushed
12:48to the background.
12:51This trend resulted in the pendulum
12:53swinging too far in favor of
12:54pharmacology this time.
12:56People began to think as if depression
12:59was only related to a serotonin
13:01deficiency. Therefore, they believed
13:03that the treatment for depression should
13:05be just like the treatment for diabetes
13:07. I had told you about this before. At
13:09least in type 1 diabetes, insulin is
13:11deficient.
13:13So, we pump that missing insulin into
13:14the body, and the job is done.
13:17Well, they thought, if the deficiency in
13:18depression is also serotonin, then we
13:20will pump serotonin into the body, and
13:21the disease will pass.
13:24This tendency was further fueled,
13:26especially as the patents for
13:28antidepressant drugs expired by that
13:30time, leading to a drop in costs.
13:35In parallel, the number of depression
13:37cases gradually increased over the years
13:39due to reasons such as the breaking of
13:41prejudices against depression in many
13:43countries, the fact that diagnosis
13:45mostly relies on subjective judgments
13:47since it cannot be detected by a simple
13:49blood test or brain scan, the increase
13:51in economic and social crises over time
13:53, and the introduction of divisive
13:55technologies like social media into our
13:58lives.
14:00In addition, with the increasing burden
14:02on healthcare systems and the
14:04difficulties in accessing treatments
14:06like psychotherapy, the rate at which
14:08physicians prescribed antidepressants
14:10like SSRIs increased significantly.
14:13That prescription explosion I mentioned
14:14at the beginning happened as a result of
14:16a combination of all these, and of
14:18course, a lot of other reasons I
14:20couldn't fit in here.
14:22Alas, new data that began to accumulate
14:24from the early 2000s started to point
14:26out that the idea that depression could
14:28be solved solely by fixing a serotonin
14:30deficiency was fundamentally flawed.
14:34Think of it this way: when you touch
14:36poison ivy, you can heal the rashes that
14:38appear on your hands and arms by
14:40applying a steroid cream, right?
14:44But the fact that the steroid works in
14:46this case does not mean that the rash on
14:48your arm is caused by a steroid
14:50deficiency.
14:51The relationship between depression and
14:54serotonin might be exactly like this.
14:57In other words, serotonin
14:58supplementation might be good for
14:59depression, but this is not enough to
15:01show that the main cause of depression
15:03is a serotonin deficiency.
15:06Indeed, when researchers prevented the
15:08dietary intake of tryptophan, which is
15:10used to make serotonin in our bodies—
15:12that is, when they artificially lowered
15:14the serotonin production in the
15:15participants 'bodies—they could not
15:17trigger depression in most of the
15:19healthy participants.
15:21However, interestingly, when the same
15:23experiment was conducted on patients who
15:26had already responded to antidepressant
15:28treatment, depression actually relapsed
15:30in some of the patients whose serotonin
15:32was depleted. So, serotonin is involved
15:35.
15:36Yes, but it does not seem possible to
15:38view serotonin deficiency as the sole or
15:40ultimate cause of depression.
15:43Furthermore, if you consider the variety
15:44of antidepressants available today, you
15:46can directly see that we cannot reduce
15:48the whole issue to just serotonin.
15:50I am going to get a bit enthusiastic
15:51here, please don't be alarmed.
15:54Think about it, today countless
15:56molecules can act on the same lock in
15:59our brains to treat the same depression
16:01, from reboxetine targeting
16:03norepinephrine reuptake to bupropion,
16:06which provides a more stimulating effect
16:09by working through norepinephrine and
16:11dopamine; from dual reuptake inhibitors
16:14, or SNRIs, such as venlafaxine and
16:17duloxetine used in patients who do not
16:19respond to SSRIs, to vilazodone,
16:23which is a 5HT1A partial agonist and may
16:26have fewer sexual side effects; and from
16:29vortioxetine, which provides benefits
16:32especially in cognitive impairment by
16:34binding to a total of five different
16:37serotonin receptors, to mirtazapine,
16:39which indirectly increases
16:41norepinephrine and dopamine release by
16:44blocking alpha-2 adrenoceptors and 5HT2A
16:47and 5HT2C receptors, or agomelatine,
16:50which suppresses 5HT2C while stimulating
16:53sleep hormone melatonin receptors.
16:57So, what would you say is the common
16:59mechanism that these different keys
17:02activate inside our brain?
17:04The answer to this question is hidden in
17:06a peculiarity you already know if you
17:08are currently taking antidepressants.
17:10Just a few hours after you swallow an
17:13SSRI pill, the amount of serotonin in
17:15your brain's neuron connections, that is
17:18, the synapses, suddenly shoots up.
17:22But even if the medication is going to
17:24work for you, it takes weeks, sometimes
17:26even months, for your mood to improve,
17:28for you to find the energy to get out of
17:30bed, or to reintegrate into life.
17:33If the issue were simply completing a
17:35chemical deficiency, as in diabetes, why
17:38would this chemical change that happens
17:41in hours only be able to heal the mind
17:43in weeks?
17:44For a long time, the answer given to
17:46this question focused on the sensitivity
17:49of receptors.
17:51For example, it was said that perhaps
17:52the reason for this delay is that
17:54autoreceptors that brake serotonin
17:56release in depression patients taking
17:57SSRIs become desensitized over time.
18:00But this idea was not enough to explain
18:02the delay on its own.
18:05For instance, in one study, when another
18:07drug that blocks these autoreceptors
18:08from day one was added to SSRI treatment
18:10, the clinical effect of the medication
18:12did not speed up significantly.
18:15This means the relationship between the
18:17effects of depression and the
18:18instantaneous chemical amount in the
18:20synaptic cleft was not as direct as once
18:22thought, but indirect.
18:24At this point, researchers began to
18:26focus on another one of the most
18:28important concepts in neuroscience.
18:31Neuroplasticity.
18:33That is, our brain's capacity to renew
18:35and change its connections, and in
18:37parallel with that, the changes
18:39experienced in patients' emotional
18:41information processing.
18:44Now, to understand the role of
18:46neuroplasticity well, we first need to
18:48understand what chronic stress and
18:50depression do to our brains physically.
18:54Today, we know very well that long-term
18:56stress disrupts our cortisol and
18:58noradrenaline systems, upsets our
19:00inflammation balances, and shakes our
19:02intracellular communication lines to
19:04their roots.
19:06We know from animal experiments that
19:08this type of stress can lead to a toxic
19:10damage called excitotoxicity by
19:12excessively increasing the amount of
19:14glutamate outside the cells. As a result
19:17, a serious pruning occurs in the animal
19:19brain in the prefrontal cortex, which is
19:21the center for decision-making, planning
19:23, and emotional regulation, and in the
19:25hippocampus, which is the memory center
19:27.
19:28Meaning the synapses there disappear,
19:30tissue volume shrinks—that is, atrophy
19:32occurs—and neurogenesis, or the
19:34production of new neurons, decreases
19:36significantly.
19:38In contrast, neurons in the amygdala,
19:40which manages our perception of fear and
19:42threat, and the nucleus accumbens, which
19:45is a part of our reward and motivation
19:47system, grow excessively—undergoing
19:49hypertrophy—trapping the brain in a
19:51constant cycle of alarm and
19:53dissatisfaction.
19:56This is precisely why chronic stress and
19:58depression are such terrible illnesses,
20:00and it is one of the strongest
20:02hypotheses explaining why the effects of
20:04antidepressants only appear after weeks
20:06.
20:08For depression to be reversed, the
20:10synaptic connections weakened by chronic
20:12stress need to be strengthened again,
20:14and that is a time-consuming process.
20:18Because the changes that long-term,
20:20intense stress creates in the brain over
20:23months, or even years, are not just
20:25about a decrease in serotonin.
20:27The brain's structure and its
20:29connections change.
20:31And reversing these is not something
20:33that can happen overnight, and mouse
20:35experiments confirm this exactly.
20:38For instance, in mice given
20:40antidepressants like fluoxetine, the
20:42circuits that trigger fear return to a
20:44younger, more flexible state.
20:46Thus, it becomes possible for fears that
20:49have settled in their brains to be
20:51erased.
20:52In other words, just as psychedelic
20:54substances—which I will explain in
20:56detail in another video—can potentially
20:59clear the congestion known as cognitive
21:01constipation and lead to mental clarity
21:04, antidepressants may also be able to
21:06remold solidified neural networks and
21:08make them reshapeable again.
21:12But unfortunately, this is not enough to
21:14get out of depression.
21:16Because even if the synapses in the
21:18brain become ready to sprout again,
21:20there must be something that ensures the
21:22brain forms these new connections in the
21:25direction of a healthy mood rather than
21:27more pessimism.
21:28Isn't that right? Otherwise, the patient
21:30would simply fall back into depression
21:32as before. There is something we know
21:33here.
21:34Individuals with depression truly see
21:37the world from behind a very dark filter
21:39.
21:41That is, when even a neutral facial
21:42expression is shown to them, while
21:44healthy brains perceive this neutral
21:46face as neutral, individuals with
21:48depression can perceive the same face as
21:50hostile or critical.
21:54Likewise, depressed individuals tend to
21:56remember negative memories from the past
21:58much more easily while ignoring positive
22:00developments or rewards, and in brain
22:02images of depressive patients, we can
22:04see that the brain regions associated
22:06with these negative feelings actually
22:08change over time.
22:11However, there is another interesting
22:12detail here.
22:14Even though clinical recovery takes
22:16weeks, antidepressants can reverse this
22:19negative perception bias I mentioned in
22:21just a few days, or sometimes even after
22:24a single dose.
22:27Moreover, this change happens before the
22:29patient has even begun to feel better.
22:32That is why sometimes, before the
22:34patients themselves notice this
22:36transformation, those around them—their
22:39family members or friends—notice it and
22:41tell the patient that they look better.
22:44Perhaps it has happened to you; as the
22:46use of the medication continues, this
22:48effect gradually increases, and people
22:49can return to normal levels.
22:53But more importantly, the knowledge of
22:55whether this shift in perspective occurs
22:57early also allows us to predict with
23:00high accuracy whether antidepressants
23:02will work for that person, even weeks
23:04later.
23:07For example, in one study, 22 out of 37
23:09patients who showed improvement in
23:11positive emotion processing in the
23:13second week of treatment showed over 50
23:16%improvement by the sixth week of
23:18clinical tests.
23:20But of the 11 patients who did not
23:22experience this shift in perception in
23:24the second week, only one was able to
23:26respond to treatment in the following
23:28weeks. This situation allows us to
23:30explain the delay between the two more
23:33clearly.
23:34Removing that dark filter from the
23:36patient's eyes is not enough to
23:38immediately eliminate the habits
23:40acquired during depression.
23:43The patient needs to re-experience the
23:44world with this new and more neutral
23:46perspective they have acquired, and the
23:48brain must relearn the world by engaging
23:50with their social environment through
23:51this new, more positive filter.
23:55For example, a small study conducted in
23:572014 showed that for an increase in the
23:59ability to recognize happy faces to
24:01translate into symptom improvement, the
24:03patients 'social environment must be
24:05strong.
24:07If the patient takes the medication but
24:10remains in an environment where they are
24:12isolated within four walls or subjected
24:14to abuse, it seems that eliminating the
24:17depressive perspective is unfortunately
24:19not enough on its own.
24:22As you can see, when it comes to the
24:24most complex organ in the universe, the
24:26brain, it is quite clear that to treat
24:28it, we need to go far beyond just
24:30boosting serotonin.
24:32But what exactly is the sequence of
24:34steps that will unlock depression?
24:36Unfortunately, we still do not know the
24:38universal answer to this. Research is
24:40ongoing.
24:42So, that is how it is.
24:44In light of everything I have told you,
24:46can we say antidepressants work?
24:49Yes, but not for everyone and not all
24:51the time. For some patients, sometimes.
24:55For instance, a massive meta-analysis
24:57from 2022 reviewing over 200 academic
25:00studies found that SSRIs provided a
25:02median improvement of about 10 points on
25:04a standard depression scale, while
25:06placebos provided a 7-point improvement
25:08.
25:10So, these drugs do not seem to have a
25:12significantly higher effect than a
25:13placebo.
25:15At least in that meta-analysis. Because
25:17there are also findings that show the
25:19exact opposite.
25:20For example, between 1990 and 2003, when
25:23SSRI use became widespread, suicide
25:25rates in the 10 to 24 age group in
25:28America decreased by approximately 29%.
25:31That is not bad at all.
25:33Let's say the reason for this was not
25:35SSRIs, but some other factor.
25:36But there is also this.
25:38The American Food and Drug
25:40Administration (FDA) decided to place
25:42warnings on these drug boxes similar in
25:44severity to those on cigarette packs
25:46after their own meta-analyses showed an
25:48increase in suicidal thoughts among
25:50children and adolescents using
25:52antidepressants.
25:54Following the placement of these
25:56warnings, there was an increase in the
25:58rate of drug poisonings, which is an
26:00indirect indicator of suicide attempts
26:02among young people.
26:04Of course, we do not know for sure, but
26:05it is thought that the reason for this
26:07is reduced access to treatment.
26:09In other words, the cost of leaving
26:11depression untreated can be much heavier
26:13than the risk posed by the medication.
26:15That is why we cannot generalize and say
26:17"these drugs do not work" just by
26:19looking at the cases that do not respond
26:21. This is extremely dangerous. Those who
26:23benefit from antidepressants experience
26:25a truly meaningful change in their lives
26:28, and this group of people is not small
26:30at all, but yes.
26:32It is also certainly not right to look
26:34only at the cases that do work and say
26:35these drugs are the definitive treatment
26:37for this disease and no other path
26:39should be sought.
26:40Research in this field needs to be
26:42supported as much as possible. Because
26:45there are still way too many things we
26:46do not know. For example, about half of
26:48those who use these drugs experience
26:51emotional blunting.
26:53In other words, the drug mechanism that
26:55should reduce pain and anxiety perhaps
26:57suppresses joy and excitement in half of
26:59the people, and this results in many
27:01people quitting these drugs.
27:04Likewise, some antidepressants create
27:06stomach or sexual problems in patients.
27:09These must definitely be solved as well
27:11.
27:12Furthermore, in addition to
27:13antidepressants, methods such as
27:15psychotherapy and neurostimulation
27:17should also be kept among the options.
27:19In our country, psychologists still face
27:22very serious structural problems
27:24stemming from appointment issues,
27:26exorbitant and unregulated fees in
27:28clinical psychology master's programs,
27:30and the lack of proper professional
27:33definitions. We cannot expect to make
27:35any breakthroughs in the much larger
27:37problems of science while we are unable
27:39to overcome even these simple issues.
27:41In other words, as a nation and as
27:43humanity, we still have a very long way
27:45to go in this regard.
27:46But it is clear that whether we are
27:49talking about depression, learning, or
27:51other issues we didn't cover today like
27:54trauma, our brain's ability to change
27:56itself throughout our lives is truly the
27:59greatest evolutionary superpower we
28:01possess. When that power slips out of
28:04control, unfortunately, it can lead to
28:06very serious tragedies. But when we
28:09learn to master it, we can learn to
28:11overcome even the most severe illnesses
28:14.
28:15As long as we know how to ignite that
28:17healing spark our brain needs to return
28:20to normal when something goes wrong,
28:22before we give up on life itself.
28:26If you enjoyed this video, I highly
28:28recommend you watch our video on male
28:30suicide as well.
28:32See you in the next video, goodbye.

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