It also enhances the production of DHEA which is also very good for boners
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Two hormones which predictably decrease with age are melatonin and DHEA, while most remain other hormones constant.
This is an important fact, yet it becomes more relevant after knowing a decline in the former causes a decrease in the latter.
This is surprisingly true. It has actually been shown experimentally that melatonin actually stimulates DHEA synthesis in the adrenal cortex (Olmez, 2003).
So it isn’t merely a coincidence but a CAUSAL event, as one is responsible for the other.
For this reason, it could be argued that the decrease of DHEA seen with aging is primarily a consequence of declining melatonin levels.
So what causes declining melatonin levels with age? Is it the progressive calcification of the pineal gland?
Yes, it is probably the calcification of the pineal gland.
Yet luckily for us modern humans, we can now supplement ourselves with as much or as little melatonin and/or DHEA as we choose.
There’s no reason to be stuck with low melatonin levels, low DHEA levels, low androgen levels, and the penile limpness that follows.
This ability to enhance DHEA synthesis could be why men with penile limpness have been found with 24% lower serum melatonin, as measured at 8 AM (Bozkurt, 2018):
Yet there are a few other things besides DHEA which can logically explain these results:
- Melatonin also causes the release of VIP in the penis, likely through calmodulin (Olmez, 2003)
- Melatonin inhibits the release of catecholamines from the adrenal medulla, almost certainly through MT1 receptors (Arangino, 1998)
- Melatonin increases nNOS expression, probably through the RORα nuclear receptor (Arese, 2012)
- Melatonin increases cyclic GMP, likely through calmodulin (Vesely, 1980)
Catecholamines are the main INHIBITORY factor in the penile firmness response, so either decreasing these or blocking α-receptors tends to remove inhibition and produce rockiness.
Cyclic GMP and VIP are both powerful vasodilators that increase blood flow to the penis.
It might then seem as if melatonin has more influence than is commonly supposed, exerting both immediate and long-term DHEA-dependent effects.
Since melatonin is affordable and is available over-the-counter, this may seem too good to be true.
For this reason, below is the evidence for these claims:
These researchers had isolated a penile bulb in vitro and had examined the effects of a few substances, including melatonin, luzindole, phenylephrine, tetrodotoxin, guanethidine, and atropine.
The penile bulb is simply the base of the corpus spongiosum, a mesh-like space that engorges with blood during the erections response.
What they had found was that, at physiological concentrations, melatonin would inhibit contractions — i.e. shrinkage — caused by both phenylephrine and a 50 Hz electric field.
They had also found that atropine did nothing, thus ruling out muscarinic receptor involvement…
…and that guanethidine could entirely prevent melatonin’s ability to relax the trabeculae.
Guanethidine is an antagonist of VIP, which is an extremely potent vasodilator (EC ≈ .03 nM).
The penis has an especially high density of VIP neurons (Polak, 1981), so much that some researchers have even considered it to be the PRINCIPLE neurotransmitter at initiating the penile response (Adaikan, 1986).
“VIP concentrations were particularly high in the pudendal arteries as well as in the ‘firmness’ tissue of the corpus cavernosum.” ―Polak, 1981
The ability of melatonin to release VIP had also been demonstrated before by others, and that β-adrenergic receptors aren’t involved either (Weekley, 1995).
So what is the target? How does melatonin do this?
One might naturally assume that melatonin membrane receptors (MT1, MT2) are responsible for the VIP release but since luzindole — an MT1/MT2 antagonist — hadn’t prevented it from occurring, there’s likely to be a different target.
Luzindole had actually inhibited the contractions, paradoxically, and to a similar extent as melatonin.
This is puzzling, and since the response was instantaneous, the slow-acting melatonin nuclear receptors (RORα, RORβ, RORγ) aren’t involved either..
Yet melatonin has 2 other cellular targets that could be responsible, calmodulin and the enzyme quinone oxidase-2 — formerly known as MT3.
Seeing as though calmodulin has been shown to associate with VIP with high affinity (Stallwood, 1992), and that melatonin and luzindole both bind calmodulin (Benítez-King, 1993), I think it’s fair to assume that calmodulin is the target in this case.
So melatonin antagonizes catecholamines — i.e. epinephrine, norepinephrine — by releasing VIP in the penis, but what makes it even more useful is that it lowers their presence in the first place:
In the pursuit of understanding why blood pressure declines at night, a research group from Italy decided to see if catecholamines change upon melatonin administration.
So they had recruited 14 healthy male subjects of average body weight, half of which were given melatonin (1mg) and the other half a placebo.
90 minutes later, their blood pressure was recorded and their blood was drawn. Perhaps what you’d expect, norepinephrine was found 21 to 22% lower in the melatonin group.
This ability of melatonin to inhibit catecholamine synthesis has recently been confirmed in vitro, and shown to occur through MT1 receptors ( Komatsubara, 2017).
This is important, as elevated norepinephrine is a prime cause of penile limpness.
This is such a well-known interaction among urologists that epinephrine is the first-line treatment for priapism (van Driel, 1991) — erections lasting longer than 4 hours.
Catecholamines are also the reason why penis shrinks in cold weather.
On the other side of the coin, α-adrenergic blockers — e.g. phentolamine, yohimbine, prazosin, apomorphine — have consistently been shown to facilitate rockiness.
So melatonin prevents the release of catecholamines to begin with, and then also inhibits whatever remains by releasing VIP.
So besides its ability to increase DHEA, we now have 2 other reasons why impotent men have 24% lower melatonin levels.
Yet if that wasn’t enough, it has been shown to do a few more things:
This was a straightforward study investigating the effects of melatonin on human keratinocytes, with special emphasis on the enzyme nitric oxide synthase.
They found that melatonin at a concentration of 1 nM would increase nNOS fourfold. This effect was specific, as the amounts of neither the iNOS or eNOS changed:
Androgens also increase nNOS in the penis, 1 reason that’s used to explain their role in maintaining the penile firmness response.
These cells had expressed many high-affinity melatonin targets that could’ve been responsible — MT2, calmodulin, quinone reductase-2, RORα…
…yet since the nNOS peaked after 6 hours, it was almost certainly occurring through the RORα nuclear receptor.
Considering the low amount of melatonin needed, it really couldn’t be anything else but a very specific receptor.
A 1 nanomolar concentration is exceedingly low, yet unbelievably it is still about 5 times higher than the nightly melatonin peak.
Melatonin is certainly 1 of the most potent hormones in the body, having a nightly maximum of only ~200 picomolar.
For this reason there’s certainly room for abuse. Melatonin tablets are available anywhere from 300 microgram to 20 milligrams, yet merely 400μg increases serum levels ninefold over the normal nightly peak (Edwards, 2011).
Luckily melatonin has a short half-life of 50 minutes, thus adding a safety factor, but the lowest dose on the market (300μg) is still more than enough.
So melatonin has a profound influence over heat regulation and reproduction, which it accomplishes by modulating blood flow in response to night/day.
It does this in a few ways, as shown above, but it also increases cellular cGMP in a variety of organs.
Cyclic GMP is another potent vasodilator and the very reason the treatment that rhymes with “Niagara” is marketed for penile limpness.
As early as 1981, very low concentrations of melatonin have been shown to increase cGTP in more than 1 organ:
This researcher had sacrificed rats and analyzed a few of their organs, including the testes, in response to melatonin.
He discovered that melatonin would increase cGTP concentrations in all organs tested, even in concentrations as low as 1 picomolar:
The author assumed that melatonin activated guanylate cyclase — the enzyme which makes cGMP from GTP — yet his experiment wasn’t conducted in such a manner as to exclude phosphodiesterase from involvement.
Phosphodiesterase is what breaks down cGMP, so inhibiting this enzyme leads towards the same result as “activating guanylate cyclase.”
Inhibiting phosphodiesterase actually appears to be the more likely mechanism, and fourteen years later it was all but proven (Faillace, 1995).
“Phosphodiesterase activity was significantly decreased by melatonin.” ―Faillace, 1995
This is also supported by the fact that phosphodiesterase type-1 (PDE1) is widely-known to bind calmodulin…
…an association so characteristic that the enzyme is commonly referred to as calmodulin-dependent phosphodiesterase.
Melatonin binds calmodulin with a Kd of 188 pM (Benítez-King, 1993), so this mechanism can explain the results.
So nearly everywhere you look, you find melatonin initiating cellular changes needed to relax arteries and increase blood flow.
Yet perhaps most importantly, melatonin stimulates the synthesis of DHEA — an androgen precursor that declines with age.
These researchers had sacrificed rats at 4 different time points and incubated their adrenals with 3 graded concentrations of melatonin: 50μM, 150μM, and 450μM.
2 hours after the melatonin addition, the adrenals were homogenized and assayed for DHEA.
Although the concentrations used were far higher than you’d ever expect in vivo, it is dose-dependent and supported by other evidence.
For instance: DHEA follows a circadian rhythm that closely matches that of melatonin (Ghiciuc, 2011).
Even though they’re both synthesized and released by the adrenal cortex, DHEA and cortisol are under the control of different regulatory factors.
Also supporting this mechanism is the finding that the key enzyme needed for DHEA synthesis — steroid 17α-hydroxylase (CYP17A1) — is upregulated in many cell lines by small concentrations of melatonin (Ya-Mei He, 2016).
This effect is blocked by the specific MT2 receptor antagonist 4-phenyl-2-propionamidotetralin, thus suggesting the target.
So melatonin has been shown to induce a wide array of biochemical changes in support of the evidence above, namely, that impotent men have 24% lower levels than controls.
I think it’s fair to assume this is not a coincidence, and that melatonin can restore the penile firmness response in humans as it’s been shown to do in rodents (Drago, 2000).
- Melatonin causes the release of VIP in the penis through calmodulin (Olmez, 2003)
- Melatonin inhibits the release of catecholamines from the adrenal medulla through MT1 receptors (Arangino, 1998)
- Melatonin increases nNOS expression through the RORα nuclear receptor (Arese, 2012)
- Melatonin increases cyclic GMP through calmodulin (Vesely, 1980)
- Melatonin increases DHEA synthesis through MT2 receptors (Haus, 1995)
Yet caution must be taken as melatonin is exceedingly potent, and it’s really only appropriate when taken at night.
The smallest dose on the market is 300μg, yet half of this may be more preferable.
This is because only 400μg melatonin has been shown to increase serum levels ninefold over the normal nightly peak:
So ultra-low-dose melatonin supplementation during the night, and DHEA supplementation during the day…
…could likely go a long way towards preventing age-related degenerative changes!
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