Hacker News Reader

Comment by ggm | Hacker News Reader

A professional I know in the field (who repudiates drugs for CBT, and so is probably biassed, but still...) says that the lack of clarity over how an antagonist and a suppressant can both be claimed to operate on the same underlying problem and have adherents, points to bad understanding of what actually causes the problem.

View on HN

I basically agree with your friend, but I'm pro-drugs for pepole who find them helpful. I very strongly suspect that the underlying "problem", like with cancer, is actually an enormous variety of problems that cluster into vaguely similar symptom groups. I am absolutely not an expert here, this is a layperson's opinion, but it's really hard to imagine that there's just one specific cause that we're treating. I think that's why different drug classes vary so wildly in effectiveness from person to person, there's a ton of underlying confounding variables that we simply don't understand.

But what we do know is that anti-depressants can be a powerful tool for helping people who aren't responsive to other types of treatment. Even if it takes some effort to figure out which one is the best fit for the underlying disorder, that's better than nothing.

Yes, but we need professionals to be more overt we are groping in the dark I think.

The recent news about why ketamine works is a very specific aha moment, they showed a focussed impact on a brain functional element which seems to re-stim negative ideation and so blocking it relieves a cycle and then permits some kind of reset. Layman's analogies.

True, but man found fire very useful for millennium before we understood it.

And as little as we know about how drugs work we know less about how CBT works.

Yes, "push a man into a fire, and end his hunger forever" useful stuff fire.

Few drugs solely act to agonize or antagonize a single type of receptor in a single part of the brain. Many of these compounds do a lot of different things, some big and some small. Anti-depressants have very complex mechanisms of action which we don't fully understand, and may not understand for a long time. They are a rough and imprecise solution to what for some is an otherwise intractable and potentially fatal problem.

Obviously therapy and other techniques should be attempted before drug prescription, but your friend is grossly oversimplifying how these drugs work and how psychiatrists portray how they work.

I grossly oversimplified what he said, and he's a trained clinical psychologist. The underlying point is exactly what you said: Anti-depressants have very complex mechanisms of action which we don't fully understand, and may not understand for a long time.

That they work is good. That they work about as well as CBT does, poses questions which as you observe goes to: Obviously therapy and other techniques should be attempted before drug prescription

With no disrespect intended to your friend, a trained clinical psychologist wouldn’t necessarily know the underlying mechanism of these drugs. The split between medical psychiatry and clinical psychology is real.

Depression and other mental illnesses are defined by a set of symptoms. Suggesting one particular cause is being disingenuous. Having said that, the whole notion of "too much" or "too little" of something like serotonin is a gross oversimplification, at best useful as a metaphor to explain things to people at a very high level.

If you want to take it a step further, think about what's causing communication via neurotransmitters to be slowed or sped up (not enough available? not being released? not being picked up by receptor?), the fact that there are multiple receptors for each neurotransmitter which drugs may or may not manipulate, the fact that there are multiple neurotransmitters (which end up affecting different areas of the brain and hence different symptoms, though some symptoms are influenced by multiple neurotransmitters), and that putting all these things together to result in the right balance of communication (not quantity of chemicals) in the brain, it would be a surprise if there weren't multiple different approaches for the "same" problem.

I don't understand the part about " an antagonist and a suppressant".

Do you mean agonist-antagonist mechanism of action of some drugs that treat the same condition?

As far as I know different drugs can work on serotonin/dopamine/norepinephrine but in different parts of the brain and produce different results.

I am a layman so probably use words inadvisably. Some drugs supress effects in the brain, some enhance. Yet both are seen to be deployed to try and treat depression. This is a very confusing signal. If the condition can present from either too much or not enough of something, what diagnostic determines which to try? What evidence do we have, of a mechanism to determine which except for "suck it and see"

I see, my intuition is that the brain is like a very complex analog amplifying station with different types of transistors, capacitors, resistors, whatever.

Drug A decreases 100ohm resistor values to 50 in a noise filter stage and "fixes" your problem with the radio.

Drug B has same 100ohm -> 50ohm effect, but in a different section of the radio and doesn't work.

Drug C increases the speaker resistance from 5ohm -> 10ohm and "fixes" your problem because you simply cannot hear the noise.

Drug D increases the microphone resistance from 5ohm -> 10ohm and the noise simply is not picked up.

Drugs A and B work the same way, drug C and D work the same way, but opposite to how drugs A and B work and they all provide the same net effect as far as I'm concerned.

This is a good analogy, because there are a lot of different biochemical pathways that can play roles in mental health. To add add to that, here's a good image of 4 of the ways a drug can effect activity at certain sites (not mental health specific, general pharmacology principles): https://commons.wikimedia.org/wiki/File:Inverse_agonist_3.sv...

Reply on news.ycombinator.com