Alexis Fernandez-Preiksa

The OGs, especially the OGs that were commenting, you know how much I love pharmacology, especially when we talk about drugs and drug design and the mechanism of action, the pharmacology.

And one thing that I love almost more than anything when it comes to pharmacology is drugs that have been taken off the market and why.

So the brain slash drug fact of today is methoqualone, also known as Quaaludes.

We're going to be fucking talking about the rise and fall of quaaludes and it's kind of like this quote-unquote safe sedative that absolutely was not safe, okay?

So I find that something so interesting about pharmacology is like how often, you know, medicine and, you know, a therapeutic drug will become such a fucking disaster and then needs to be pulled off the market because – often because of abuse.

You know, there'll be well-intended –

you know, use for that drug and the way it works actually works how they intend it to work.

But then because the side effects are so dangerous or because the misuse of that drug can be so dangerous and when in the wrong hands or when people use it recreationally, then it's borderline a catastrophe and then it has to be kind of pulled off.

But quaaludes were marketed in the 1950s and 60s as a, believe it or not, safer alternative to barbiturates.

And I've done a whole brain fact on barbiturates, but I will kind of brush over them in a second.

But yeah, they eventually became, after that, one of the most famous recreational sedative drugs of the 1970s.

And the name Quaalude...

actually comes from the phrase quiet interlude, which suggests like peaceful, restful experience for users who wanted to treat insomnia or anxiety.

So methaqualone, which is, you know, quaaludes are methaqualones.

It's a sedative hypnotic drug.

So it works as a central nervous system depressant.

And a lot of the drugs that I talk about, especially when you're treating things like anxiety or insomnia or other related things, work as a central nervous system depressant.

You are reducing activity in the CNS instead of being something that's going to increase activity.

So you're depressing that activity and you're enhancing signaling at the GABA-A receptor complex.

I'll go into that in a second.