SSRIs as Anticoagulants: Plausible?

Factual Questions
1

This article from Scientific American (“Why? The Neuroscience of Suicide” February 2003) states platelets have serotonin receptors. It states nobody knows why.

With that trifling investment of fact, I’ve come up with an interesting hypothesis.

Platelets have serotonin receptors because the absence of serotonin indicates mental stress. The opposite is true: The presence of serotonin indicates mental relaxation. So, I think, it’s an adaptation: Serotonin makes the platelets less sticky, because when it’s in abundance you are relaxed and less likely to be injured. When you’re stressed, serotonin levels drop and the platelets move into `ready mode’. If they were always in ready mode, we’d be dropping dead of strokes a lot more often as those always-sticky platelets clump in random locations throughout our bloodstream.

Okay, that’s leap one. The next one is more of a brief hop, if the leap leads one to solid ground.

SSRIs are Selective Serotonin Reuptake Inhibitors. That is, they effectively increase the serotonin levels in your body by preventing neurons from consuming it quite so quickly. They work wonders against depression, which is linked to low serotonin levels, and have become the next Big Thing in psychiatric phamachology under trade names like Prozac and Paxil.

So, if low serotonin levels make your blood clot (leap one), and if SSRIs would increase serotonin levels enough to make a difference (leap two, smaller than the first), wouldn’t SSRIs work as anticoagulants? There are the old anecdotes about people being more prone to strokes and heart attacks when stressed. Maybe that’s because clotting, a major factor in both events, is linked to stress, which is heavily linked to low serotonin levels.

If anyone has done serious research in this area, I’d be glad to know it. If I’m spewing more shit than a goose with a leaky colostomy bag, I’d be glad to know that, too.

And if anyone wants to offer me a huge research grant, my email address is in my profile.

2

My gut reaction is colostomy bag.

I don’t dispute your logic. It’s pretty stressful having a huge leaking wound and maybe serotonin and stress play a small role in platelet activity levels. Makes sense to me.

The role an SSRI might have would be pretty small. If it was not, you would expect to see increased bleeding and objective measures of bleeding (INR, PTT, bleeding time) in patient’s on Prozac, etc. These are not common enough to be included in the drug monograph but were almost certainly studied during beta-trials. There is no reason to believe SSRIs would replace currently used anticoagulants.

3

Okay. That makes sense. I knew I was going out on a limb.

4

Don’t be too hard on yourself.

I think you’ll be interested in at least the introductory paragraphs of this paper.

Likewise, this abstract is intriguing.

5

Thanks for the consideration and the linkage. I knew serotonin played some role in clotting. It made my day to see that my harebrained idea actually has some basis in reality.

Hypothetical (that is, not even dignified with the appelation theoretical because it’s completely untested) medicine is only slightly less effective than phrenology, but I still find it amazingly interesting to toss ideas around in my head.

6

The idea is a good one. Having a reasonable mechanism is a very important part of scientific plausibility. It just doesn’t always pan out in the real world. And fifty pecent of the medicine I use could be out the window in twenty years, so you may be laughing last.