T Nation

Serotonin & Test - Inverse Relationship

Ray Peat is a biochemist who specializes in nutritional questions. I don’t know what to make of this, but he claims an inverse relationship between serotonin and testosterone. Read and post about what you think of this:


Seems like we are just starting to learn.

Fascinating stuff. Thanks!

Hmm, eat your Gelatin seems to be the message.

I think I might start doing that.

[quote]Elaikases wrote:
Hmm, eat your Gelatin seems to be the message.

I think I might start doing that.[/quote]

That, and eat your coconut oil.

Anyone get any other “take homes” from this article?

These articles are rather rambling; I wish this guy would write summaries at the end.

I don’t think it was rambling…but certain parts DID get tough to follow.

I think many of us (and I’m including myself) have become lazy and want to be told what to do, without know WHY you’re doing it.

Good article.

It seems wrong that the linked material has no discussion of the context of SSRIs.

LEF.org seems to state the opposite:




Given the conflict, I will not take any of Ray Peat’s money to the bank. Yes, too much seratonin is a problem, but that does establish the need to reduce or avoid.

Too many of Ray’s discussed issues are pointless. Example - hardening of connective tissue. This is also a well known effect of glycation from elevated blood sugars. That is part of aging and not exclusive to an effect of seratonin.

I’ve been on Zoloft, an SSRI designed to increase serotonin since april. In that time, I’ve gone from 250 to 315 on bench, 475 to 525+ on deadlift, and 365 w/ wide stance to 440 narrow stance and deep on squat. My bodyweight went from 200 to 240 in that time period, and my body fat is acceptable.

I take the drug for OCD and gastroparesis. Symptoms have been alleviated SIGNIFICANTLY. Part of the reason for the surge in progress is because now that my anxiety is lowered, I no longer get nauseous or lose appetite quickly.

Is it somehow hurting my testosterone levels? I don’t think so.

Certainly his points deserve further consideration. I don’t know exactly what he thinks optimal levels of serotonin would be. I do know that there is a school of thought that claims there is no relation between serotonin levels and depression. I don’t know much about that though. I will research it a bit.

Anyway, why do SSRIs OFTEN trigger Erectile Dysfunction in a lot of men? Does this have to do with lowering the testosterone or some other mechanism?


For more then 15 years, there has been speculation on the significance of serotonergic pathways in the control of male sexual function, especially in the maintenance of penile flaccidity and the initiation of detumescence. However, only a few in vivo studies on peripheral serotonergic transmission have been carried out. The aim of the present study was to evaluate further the effects of serotonin (5-HT) on isolated human erectile tissue and to detect serum levels of 5-HT in the systemic and cavernous blood taken during different penile conditions from healthy males.

The effects of 5-HT on isolated human corpus cavernosum (HCC) were investigated using the organ bath technique. A total of 41 healthy, adult male subjects were exposed to erotic stimuli in order to elicit penile tumescence and rigidity. Whole blood was simultaneously aspirated from the corpus cavernosum and the cubital vein during different penile conditions. Serum levels of 5-HT (ng/ml) were determined by means of an enzyme-linked immunosorbent assay.

The cumulative addition of 5-HT (0.001?10 µM) induced contraction in the isolated HCC strips. The contractile response was abolished in the presence of 5-HT1α-receptor antagonist NAN-190. No attenuating effect of 5-HT was observed on electrically induced relaxation of the tissue. Moreover, amplitudes of relaxation remained unaltered in the presence of NAN-190.

In the healthy volunteers, a significant increase in 5-HT levels was detected in the cavernous serum from flaccidity (113±62) to tumescence and rigidity (140±69 and 141±54, respectively), followed by a decrease in the detumescence phase (123±79). Changes in 5-HT levels in the systemic serum were less pronounced. Under all penile conditions, systemic 5-HT levels were higher than those registered in the cavernous serum.

Although 5-HT does not appear to be involved in postsynaptic transmission in the HCC, our results may provide evidence for a physiological significance of 5-HT in the control of penile flaccidity and detumescence. Thus, our findings may give a rationale for the use of 5-HT antagonists in the pharmacotherapy of erectile dysfunction