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Comment by cryoshon | Hacker News Reader

The entire "chemical imbalance" model is a lie designed to make drugs easier to sell, and here's a simple pair of facts which prove that the science is bunk:

SSRIs increase levels of serotonin at the synapse when administered by preventing serotonin re-uptake and recycling, improving mood.

SSREs decrease levels of serotonin at the synapse when administered by enhancing serotonin re uptake and recycling, improving mood.

Two drugs with opposite effects achieve the same qualitative result, even though it can't be said that they produce similar quantitative results. Thus, vastly different quantitative profiles are correlated with the same qualitative results; X + 1 = X - 1.

On top of that, there's no way to even measure levels of synaptic neurotransmitters in vivo.

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There are multiple serotonin receptor types, and the "selective" types of reuptake modifiers don't affect all of them all the time in all people.

That said, too much or too little serotonin absorbed by a specific set or another can have wildly different effects.

Too much serotonin is not a good thing. So you need to balance it. For some people, this means SSRIs, for some it means SSREs. That's the explanation for the imbalance model, and it does make sense given the science.

It's ridiculous to talk about "balance" when you can't actually measure any of the quantities you're trying to balance and don't even have a clear picture of what "balance" looks like qualitatively, never mind quantitatively.

Sure, blast a brain with drugs that aren't well understood and it'll behave differently, maybe "better" than before, relatively speaking-- but that's not a scientific model so much as a pragmatic clinical solution.

It's ridiculous to talk about "balancing" the flavors of your soup when you can't actually measure any of the quantities you're trying to balance and don't even have a clear picture of what "balance" looks like qualitatively, never mind quantitatively.

Sure, dump in a bunch of spices that aren't measured and it'll taste different, maybe "better" than before, relatively speaking--but that's not a scientific model so much as a pragmatic cooking solution.

What is your point? That is definitely not a scientific model.

Yes. This is dog.

It's obvious you don't know very much about serotonin. Here's why:

SSRIs bind to the serotonin transporter SERT. The 'selective' part means that it has a much higher affinity for SERT than other monoamine transporters (e.g., DAT or NET). Although you're correct that there are various serotonin receptor subtypes, there is only one known SERT (there is only one gene).

SSRIs do exhibit extremely weak affinity to serotonin receptors but it is so low that it doesn't matter which subtype has a higher affinity than another. If you want to latch on to 5HT receptors with interesting ratios and affinities, the correct psychiatric drug would be an antipsychotic.

Please stop defending the chemical imbalance model when you do not understand the science at all. Thank you.

I assume when you say SSRE you are talking about tianeptine? Its affinity for SERT is low and its primary target is believed to be elsewhere.

Do those two drugs achieve the same effect in the same patients? There are plenty of treatments with opposite effects that achieve the same qualitative result, in different patients with different conditions that merit different treatments. Could that simply be the case here, or do both kinds of drugs typically work in the same people?

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