Thread Rating:
  • 0 Vote(s) - 0 Average
  • 1
  • 2
  • 3
  • 4
  • 5

Serotonin & depression: a controversy that never was

#1
C C Offline
https://www.openmindmag.org/articles/ser...-never-was

INTRO: The media went crazy when a study showed low serotonin doesn’t cause depression—but this was something scientists had known all along. The confusion caused some patients to go off effective psychiatric medications, exposing an information gap it’s been hard to bridge. We can do better, and here’s how.

EXCERPTS: For decades now, common wisdom has held that the more serotonin bathing your brain, the less depression you experience and the sunnier your mood and outlook on life. Doesn’t that explain the mighty power of Prozac and other selective serotonin reuptake inhibitor (SSRI) antidepressants, from Zoloft to Paxil, which boost serotonin in the brain?

The reasoning seems to make sense. Serotonin is a neurotransmitter—a chemical that carries messages between brain cells—involved in many functions throughout the brain and body. For instance, serotonin plays a role in heart and gut function and helps regulate sleep and wakefulness. Given the efficacy of SSRIs for some, it would seem safe to assume that low serotonin levels create a chemical imbalance in the brain that can lead to depression.

Last summer, that belief appeared to be upended by a research paper from scientists at University College London. Published in the respected scientific journal Molecular Psychiatry, the report concluded that low serotonin is not a cause of depression, creating more controversy than any psych paper in recent memory.

As the story surged, public outrage grew. Readers began to ask: If low serotonin doesn’t cause depression, then why are so many of us treating it with SSRIs? How could doctors have been so wrong?

As a neuroscientist, I found it frustrating to watch this unfold. Although it seemed shocking and groundbreaking, this paper actually did not tell us anything new about depression. The researchers had not run any experiments or uncovered something novel about the condition. Rather, they had simply summarized the scientific research that had already existed on depression for decades.

Let’s back up a bit. In the 1950s...

[...] So, what exactly is going on here? How can SSRIs be helping if low serotonin isn’t the problem? The (perhaps unsatisfying) answer is that in the brain, things are hardly ever as straightforward as this. ... serotonin levels don’t need to be low for SSRIs to be helpful in treating depression; increasing serotonin could alter the function of some other, downstream system, which then leads to improved mood.

[...] Here’s another way to think of it: If you spend six hours squinting at a computer screen at work, you might have a headache when you get home. You go to the medicine cabinet and take some Tylenol to get rid of it. In this case, the root issue is that your facial muscles have been overworked and spasming, but the Tylenol acts on a different system in your body to simply blunt the pain. It does not relax your muscles, but it does stop your experience of pain, and that’s all you really wanted. SSRIs could be acting in a similar way, addressing the problem indirectly.

[...] Despite all this, the story came as a huge shock to those outside the field and stirred public outrage. The reason? An unfortunate disconnect between science and the public...

[...] So, what is the solution? Perhaps scientists need to be more careful with what they publish. Or maybe media outlets need to be more accurate in their reporting. But is it really the responsibility of either side alone? In an ideal world, the dialogue between scientists and journalists would grow, allowing each side to draw on the strengths of the other... (MORE - missing details)
Reply
#2
Magical Realist Offline
Quote:Here’s another way to think of it: If you spend six hours squinting at a computer screen at work, you might have a headache when you get home. You go to the medicine cabinet and take some Tylenol to get rid of it. In this case, the root issue is that your facial muscles have been overworked and spasming, but the Tylenol acts on a different system in your body to simply blunt the pain. It does not relax your muscles, but it does stop your experience of pain, and that’s all you really wanted. SSRIs could be acting in a similar way, addressing the problem indirectly.

That's a good analogy. Might also explain how boosting your serotonin can help with temporary circumstantial depression, like the death of a loved one. The cause of the depression isn't eliminated but it's power over the brain is lessened to get you thru it. Another of many medical instances of treating the symptom over the cause.
Reply
#3
Syne Offline
That is a good analogy. It's an analogy about treating the symptom in lieu of addressing any root cause. Not only that, but, as admitted in the article, they don't even know how SSRIs accomplish any results at all. Saying SSRI's "could alter the function of some other, downstream system," without understanding the efficacy, or even which system may be involved, means you're effectively relying on luck in order to avoid doing the work to address the actual issues.

Although the early antidepressant trials which included severely ill and hospitalized patients showed substantial drug-placebo differences, these robust differences have not held up in the trials of the past couple of decades, whether sponsored by pharmaceutical companies or non-profit agencies.
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4592645/

Reply
#4
Magical Realist Offline
I see no problem with treating the symptom. We do that all the time with pain medications. Until we discover the root cause of depression (if there is one) it suffices to lessen its effect on the brain by boosting serotonin levels.
Reply
#5
Syne Offline
We know how to treat depression itself, instead of just the symptom. But it requires the individual to put in the work in therapy.
So many prefer a lifetime of quick fixes rather than the work.
Reply
#6
Magical Realist Offline
"Research shows that the hippocampus is smaller in some depressed people. For example, in one fMRI study published in The Journal of Neuroscience, investigators studied 24 women who had a history of depression. On average, the hippocampus was 9% to 13% smaller in depressed women compared with those who were not depressed. The more bouts of depression a woman had, the smaller the hippocampus. Stress, which plays a role in depression, may be a key factor here, since experts believe stress can suppress the production of new neurons (nerve cells) in the hippocampus.

Researchers are exploring possible links between sluggish production of new neurons in the hippocampus and low moods. An interesting fact about antidepressants supports this theory. These medications immediately boost the concentration of chemical messengers in the brain (neurotransmitters). Yet people typically don't begin to feel better for several weeks or longer. Experts have long wondered why, if depression were primarily the result of low levels of neurotransmitters, people don't feel better as soon as levels of neurotransmitters increase.

The answer may be that mood only improves as nerves grow and form new connections, a process that takes weeks. In fact, animal studies have shown that antidepressants do spur the growth and enhanced branching of nerve cells in the hippocampus. So, the theory holds, the real value of these medications may be in generating new neurons (a process called neurogenesis), strengthening nerve cell connections, and improving the exchange of information between nerve circuits. If that's the case, depression medications could be developed that specifically promote neurogenesis, with the hope that patients would see quicker results than with current treatments..."--- https://www.health.harvard.edu/mind-and-...e%20events.
Reply
#7
Syne Offline
Brain structures have been shown to change due to behavior through neuroplasticity. But dedicated materialists just assume, without any demonstrable evidence, that the reverse causation must be true. That's conflating correlation with causation, and not how science is done. Saying hippocampus size and depression are correlated doesn't speak to causation...unless you can demonstrate the mechanism.
Reply
#8
Magical Realist Offline
We don't know the causal mechanism of pain either but we do know it correlates to certain adverse effects in the body. Inflammation, tumors, injuries, neural stimulation and various brain activities all correlate to pain, and that is sufficient for us to treat it even if it is but a symptom of the problem. The same with depression. We may not know its mechanism, but we know enough of its correlations to genetically-determined brain structure and synaptic brain chemistry to be able to treat it successfully.
Reply
#9
Syne Offline
Wait, what? We don't know the mechanism of pain? You sure you don't want to rethink that statement?

With pain, like depression, you either treat the symptom, endlessly, or you find out what's really wrong. A bandage versus a cure. Treating the symptom is lifelong dependency on, usually, increasingly powerful drugs...with the looming threat of more severe rebound pain should you ever lapse.

If you were treating the depression, itself, you wouldn't need an endless prescription of meds. You'd develop better self-awareness and coping strategies. But that takes work, and people nowadays just want easy fixes.
Reply
#10
Magical Realist Offline
Quote:Wait, what? We don't know the mechanism of pain? You sure you don't want to rethink that statement?

We know that pain is a construct of the brain. Simply localizing its origin to some part of the body that the brain refers it to like your back or your leg isn't really understanding the mechanism of pain. We have a long way to go towards explaining how pain is produced in the brain. But that doesn't keep us from being able to treat it with medications. Same with depression.
Reply


Possibly Related Threads…
Thread Author Replies Views Last Post
  Cannabis does not help depression, anxiety or ADHD + The male infertility timebomb C C 2 350 Oct 29, 2019 05:00 PM
Last Post: C C



Users browsing this thread: 1 Guest(s)