The Night-Time Blueprint for Lasting Erectile Function: How Optimising Nocturnal Erections Can Reverse ED

(and why they also matter for penis enlargement)

Introduction and TLDR: The Role of Nocturnal Erections in Erectile Health

Most of us are vaguely aware that we experience erections during sleep, but few appreciate just how vital these nighttime events are to overall erectile function. These spontaneous, unconscious erections—known as ‘Nocturnal Penile Tumescence’ (NPT) in medical literature—are not just a quirky physiological phenomenon. They are, in fact, one of the most important factors in preserving erectile tissue integrity, supporting long-term function, and reducing the risk of erectile dysfunction (ED). Oh, and if you’re a young guy you might suffer from the same misconception I had: That nocturnal erections are caused by erotic dreams or being horny when you fall asleep. :) Nope. They happen because of parasympathetic nervous system activation or “tone” as we say, which happens to coincide with the more superficial phase of sleep that we are in when we dream, and they are therefore independent of the content of our dreams. 

The traditional view of nocturnal erections is that they are merely an ‘epiphenomenon’—a byproduct of REM sleep with no real functional importance. However, emerging evidence suggests this is entirely incorrect. Nocturnal erections are not just a reflection of erectile health; they are central to keeping it intact. Their frequency, duration, and rigidity directly impact penile oxygenation, smooth muscle preservation, and endothelial function. When nocturnal erections become infrequent or weak, the penis is deprived of critical oxygenation cycles, leading to pathological changes such as smooth muscle atrophy, fibrosis inside the corpora cavernosa, and veno-occlusive dysfunction. In short, losing nocturnal erections is not just a symptom of ED—it is one of its root causes.

This raises an important question: If the loss of nocturnal erections contributes to ED, could restoring them reverse or prevent it? Research strongly suggests the answer is YES! Clinical and preclinical studies indicate that increasing nocturnal erections—particularly through the use of phosphodiesterase type 5 inhibitors (PDE5i) like sildenafil—can lead to long-term improvements in erectile function. Notably, nightly dosing of PDE5 inhibitors appears to produce effects that persist long after stopping treatment (months!), outperforming traditional "on-demand" use. Let me explain that last point: Taking Viagra now and then before sex does not confer nearly as many benefits to erectile function long term, as taking a PDE5i before bed every day. Another insight from the research I will present here—or perhaps I should say a natural inference from the research—is that the “milking” protocol that I have been such a vocal opponent of really is a fantastic method for maintaining or recovering penile health, since it circulates fresh blood through the penis in a manner that mimics nocturnal erections—or potentially one-ups them. Doing several short sessions of rapid interval pumping every day will be my protocol for the rest of my life, since it is probably just as beneficial for long term erectile health as cardio and good nutrition. 

That’s the gist of this whole post, so if you are in a hurry and don’t need to know the details, you can stop reading here. Taking Viagra or better yet Cialis before bed can help you recover from ED, or stave it off. Throw in some Citrulline, Arginine and NAC into that protocol while you are at it. But if you are not in a hurry and want to know the details, there’s plenty of detail to come. 

This article will explore why nocturnal erections are essential for penile health, the mechanisms by which their loss contributes to ED, and the compelling evidence that nightly PDE5i use can induce lasting physiological improvements—potentially reversing ED rather than merely treating its symptoms. I will also give some detailed thoughts about the benefits of certain PE exercises mimicking the effects of nocturnal erections, and how the risks of certain other exercises can be offset by improving nocturnals. And for good measure, I threw in some lifestyle interventions for "EQ Maxxing" as the cool kids say.

Ok, brew a cup of tea or coffee, lean back in your armchair and focus, because this will get progressively more detailed from here... :)

An important Question: Correlation or Causation?

A common argument against the idea that nocturnal erections play a causal role in erectile function is this: “Aren’t poor nocturnal erections just a symptom of ED rather than a cause?” It’s a fair question—after all, men with worsening erectile dysfunction (ED) often report fewer and weaker nocturnal erections. This has led many to assume that the loss of nocturnal erections is merely a consequence of declining erectile function, not an active contributor to it. But is this really the case?

To answer this, we need to first understand the difference between correlation and causation—a distinction that is often overlooked in discussions about ED. Many of you know this already, of course, but I write not only for people with a BSc-degree but also for people with no prior knowledge, so here goes: Correlation means that two variables change together, but it does not tell us whether one directly influences the other. For example, ice cream sales and drowning incidents both increase in the summer, but one does not cause the other—they are simply correlated because both are influenced by temperature. One of my favourite ‘spurious correlation’ examples to give is the positive correlation between how many storks live in a region, and the rate of childbirth in that region. Ten points to the reader who can figure out the underlying cause of the correlation without googling for the answer. Correlation can show up for any number of reasons. 

Causation, on the other hand, implies a direct mechanism where one factor actively drives changes in another. In the case of nocturnal erections and ED, the key question is this: Does erectile dysfunction cause a loss of nocturnal erections, or does the loss of nocturnal erections contribute to erectile dysfunction? The answer is—drumroll please… Both!

Yes, when a man develops ED, his nocturnal erections often suffer. But crucially, the reverse is also true: when nocturnal erections are impaired or absent for extended periods, the penis undergoes physiological changes that actively worsen erectile dysfunction. This is not just theoretical; studies have shown that prolonged reductions in nocturnal erections lead to:

Smooth muscle atrophy – The corpora cavernosa rely on regular blood flow to maintain smooth muscle integrity. Without frequent erections, smooth muscle is gradually replaced by fibrotic tissue, reducing the penis’ ability to expand. Prolonged flaccidity leads to outright SMC apoptosis (cell death). 

Endothelial dysfunction – Nocturnal erections are a major driver of endothelial nitric oxide (NO) production, which is completely essential for proper vasodilation and erectile function. One mechanism involved is the internal stretching stimulus of erections, which can upregulate endothelial nitric oxide synthase (eNOS)—the enzyme responsible for catalysing NO production from arginine. When nocturnal erections decline, endothelial health deteriorates. The endothelium becomes less responsive, leading to progressive vascular impairment.

Veno-occlusive dysfunction (VOD) – The venous trapping mechanism that keeps blood in the penis during an erection becomes less effective in the absence of regular nocturnal erections, leading to weaker and shorter-lasting erections. This is a downstream effect of smooth muscle atrophy and endothelial impairment; when the corpora cavernosa fail to fully expand, the venous trapping mechanism cannot function properly.

In other words, nocturnal erections are not just an indicator of erectile health—they are a necessary mechanism for preserving it. When they stop occurring regularly, ED doesn’t just remain static—it progressively worsens.

This distinction between correlation and causation is important because it shifts the way we should think about treating ED. If nocturnal erections only reflected erectile function, then trying to restore them would be pointless. But if nocturnal erections are a key driver of erectile health, then restoring them—especially through interventions like nightly PDE5 inhibitor use—could have profound, long-lasting benefits.

In the next sections, I will look a little deeper into why nocturnal erections are so important for maintaining erectile tissue health and how increasing their frequency can lead to real, physiological improvements in erectile function—ones that persist long after treatment ends. I will basically explain once again how lack of nocturnal erections will cause endothelial dysfunction, smooth muscle atrophy and fibrosis, and as a result veno-occlusive dysfunction, but this time in greater detail. Feel free to skip to part 2 if you feel you don’t want more detail. 

PART 1: Why Nocturnal Erections Matter for Penile Health

The Role of Oxygenation in Erectile Function

One of the most overlooked aspects of erectile health is the role that oxygenation plays in maintaining the structural and functional integrity of penile tissues. The corpora cavernosa, which make up the bulk of the erectile tissue, consist of vascular smooth muscle and endothelial cells that require regular exposure to oxygen-rich blood to remain healthy. Nocturnal erections (NPT) serve an important homeostatic function by ensuring that these tissues are periodically flushed with oxygenated blood throughout the night.

During the flaccid state, the penis exists in a state of relative hypoxia (low oxygen tension) due to low arterial inflow and limited cavernosal expansion. In contrast, an erection—whether induced by sexual arousal or occurring spontaneously during REM sleep—creates an initially high-flow state, increasing intracavernosal oxygen tension from venous levels (~25–30 mmHg) to arterial levels (~90–100 mmHg). Oxygen tension refers to the partial pressure of oxygen (pO₂) in a specific environment, such as within tissues or blood vessels, essentially measuring how much oxygen is available for biological processes. Although the high-flow state tapers off as the veno-occlusive mechanism engages, the high cavernosal pressure is retained, which maintains a high partial pressure of oxygen for quite some time. This is possible because the penile tissues do not demand as much oxygen as other tissues and organs; hence, the oxygen-rich blood, once trapped, continues to sustain elevated oxygen tension even when arterial inflow diminishes.

This oxygen influx is essential for several reasons:

Endothelial Health and the Role of eNOS

The endothelium plays a key role in erectile function by releasing nitric oxide (NO). NO is synthesised by endothelial nitric oxide synthase (eNOS) from arginine, and it sustains an erection by activating guanylate cyclase. This enzyme catalyses the conversion of GTP to cyclic guanosine monophosphate (cGMP), which in turn promotes smooth muscle relaxation and further arterial dilation—both vital for the maintenance of the erectile state. (I am glossing over the detail that neuronal nitric oxide synthase (nNOS) from intracavernosal nerve endings initially triggers the process, with the endothelium then taking over by utilising eNOS to sustain elevated NO levels.)

Top level understanding: 

Regular nocturnal erections help upregulate eNOS activity, maintaining the endothelium’s ability to generate sufficient NO when needed for arousal-induced erections. Reduced NO bioavailability is a hallmark of endothelial dysfunction, which is one of the earliest and most significant contributors to age-related erectile dysfunction and vasculogenic ED.

A slightly deeper dive on eNOS up-regulation: When an erection occurs, the surge in arterial inflow produces mechanical shear stress on the endothelial cells lining the cavernosal sinusoids. This mechanical stimulus triggers intracellular signalling cascades, including the activation of kinases such as Akt, which phosphorylates eNOS at specific serine residues, thereby enhancing its catalytic activity. They keep eNOS happy and healthy and in its most active form. An addition to this, shear stress can induce the transcription of the eNOS gene, leading to increased enzyme expression. Expression here means “making more of”. Over time, these repeated episodes of shear stress help to maintain or even boost the endothelial cells’ capacity to produce NO, which ensures that sufficient vasodilatory signalling is available when arousal-induced erections are required. Nocturnal erections are what enable you to have daytime erections, to put it in oversimplified terms. 

Reduced NO bioavailability is multifactorial in its aetiology (causes). One major contributor is the increased production of reactive oxygen species (ROS), which can stem from poorly functioning mitochondria, among other sources. Under normal conditions, mitochondria generate ROS at low levels (in the process of oxidizing fuel to convert AMP and ADP to the energy currency ATP); however, in ageing or in disease states, mitochondrial dysfunction can lead to excessive ROS generation (such as in covid infections, actually — the reason for “covid dick”). These ROS, particularly superoxide anions, can rapidly react with NO to form peroxynitrite, which is a potent oxidant that not only reduces NO levels but can also damage the endothelium and further impair eNOS function. (If you are paying attention and reading with your brain engaged, you will realize that this is the start of a vicious cycle). This process is sometimes exacerbated by a decrease in the availability of essential cofactors such as tetrahydrobiopterin (BH4), which is necessary for proper eNOS activity. When BH4 is depleted or oxidised, eNOS can become “uncoupled” and produce superoxide instead of NO, further contributing to oxidative stress and a vicious cycle of endothelial dysfunction. u/Semtex7 and I have both written about supplements which can aid the master antioxidant glutathione in scavenging ROS so as to prevent NO from being turned into peroxynitrite and prevent BH4 from being oxidised. I’m too lazy to link them here - go find the articles in the wiki. :) 

In brief summary before we go on; while regular nocturnal erections provide beneficial mechanical stimuli that upregulate eNOS and preserve NO production, conditions that promote mitochondrial dysfunction and excessive ROS formation undermine NO bioavailability. This imbalance is a key factor in the development of age-related erectile dysfunction and vasculogenic ED. 

There are many risk factors we can control: Smoking, alcohol, high intake of fructose or disaccharides containing fructose or high-fructose corn syrup and similar, poor cardiovascular health, the systemic inflammation and poor mitochondrial function that are the hallmarks of metabolic syndrome (the root cause of poor appetite control, obesity, diabetes type 2, etc) - many lifestyle factors are at play here. Supplements that support the function of glutathione, act as antioxidants, and suppress systemic inflammations are the best friends of erectile function. 

That’s it for eNOS and endothelial cells - let’s move on to the next key cell type: the smooth muscle cells (SMCs).

Smooth Muscle Integrity and the Prevention of Fibrosis

Cavernosal smooth muscle is indispensable for erectile function. In the absence of adequate mechanical stimulation, the smooth muscle can undergo detrimental remodelling. Prolonged periods without proper activation—such as when nocturnal erections are impaired—can lead to muscle atrophy, whereby these specialised cells lose their contractile capability, and they are progressively replaced by fibrotic, collagen-dense tissue.

Fibrosis is not merely a passive replacement of functional tissue; it actively undermines the mechanical properties of the corpora cavernosa. As collagen accumulates inside the CC, the tissue loses its compliance and elasticity, which are necessary for the expansion to happen during an erection. The loss of these properties makes it more difficult for the penis to fully engorge with blood, resulting in weaker erections that are both shorter in duration and less rigid. If the CC can’t inflate fully due to being fibrotic, they simply can’t properly compress the venules against the tunica, and you get venous leak or Veno-occlusive dysfunction (VOD). 

With VOD, blood escapes too rapidly from the erectile tissue, leading to an inability to sustain an erection. This leakage is a common finding in conditions like “soft glans syndrome” and is often observed in age-related erectile dysfunction, as well as in cases associated with diabetes.

A key mediator of this fibrotic transformation inside the CC is the upregulation of transforming growth factor-beta 1 (TGF-β1). Under conditions of chronic hypoxia or disuse, as might occur with long-term impairment of nocturnal erections, TGF-β1 expression increases. This cytokine drives the conversion of resident fibroblasts into myofibroblasts—cells that synthesise large amounts of collagen and other extracellular matrix proteins. The resultant deposition of collagen alters the structural matrix of the erectile tissue, further inhibiting the necessary distensibility of the corpora cavernosa. In PE we are used to thinking of collagen synthesis as a “good thing”. And it is - in the tunica! But not inside the CC.  

Evidence from both animal models and clinical observations exists for the phenomenon I’m describing. In rodent studies, sustained hypoxia led directly to heightened TGF-β1 levels, followed by notable smooth muscle loss and collagen deposition. (Lv, B. et al. (2014). Phenotypic transition of corpus cavernosum smooth muscle cells subjected to hypoxia. Cell and Tissue Research, 357, 823 - 833 and in Lü BD et al, [Hypoxia promotes corpus cavernosum smooth muscle cell apoptosis in SD rats] (in Chinese). Zhonghua Nan Ke Xue. 2009 Nov;15(11):990-3)

Similar remodelling has been documented in men with long-term spinal cord injuries, who experience diminished reflexogenic and nocturnal erections, and in patients following radical prostatectomy. In these cases, the absence of regular mechanical stimulation accelerates fibrotic remodelling. Two cases perhaps worthy of special mention since they are so common, are (1) men with untreated sleep apnea, who experience disrupted sleep cycles and reduced nocturnal erection and who have a significantly higher incidence of cavernosal fibrosis and ED​, and (2) diabetic men, where the combination of vascular dysfunction and reduced nocturnal erections accelerates the onset of collagen remodeling and VOD, making them less responsive to PDE5 inhibitors over time. 

In brief summary again before we go on, the preservation of cavernosal smooth muscle is critical to maintaining effective erectile function. Regular physiological activation through nocturnal erections not only prevents atrophy but also guards against the fibrotic processes that render the erectile tissue less capable of achieving full rigidity. Regular penile activity: good. No-Fap: sheer idiocy. Use it or lose it. 

If you take nothing else away from this section, let it be this: The penis needs nocturnal erections to prevent long-term deterioration. The absence of these erections is not just a temporary dysfunction—it is a progressive pathology that leads to fibrosis, venous leakage, and irreversible structural changes in the erectile tissue. (Well, perhaps not so irreversible - CF602 and a protocol of milking for oxygenation and stretching stimulus could help, as could shockwave treatment and PRP injections. But unless aggressively treated, it’s a progressive and irreversible pathology that does not get better on its own). 

With this in mind, it becomes clear why interventions aimed at restoring nocturnal erections—such as nightly PDE5i use—are not just a temporary fix, but massively important for reversing or preventing the progression of ED.

In the next section, we will explore how nightly PDE5 inhibitor use can actively preserve and even restore erectile function, reversing the damage caused by the absence of nocturnal erections.

PART 2: The Science of Nightly PDE5 Inhibitor Use

The Evidence for Nightly PDE5i Over On-Demand Use

The standard approach to phosphodiesterase type 5 inhibitor (PDE5i) therapy for erectile dysfunction (ED) has long been “on-demand use” — taking the drug shortly before sexual activity to more easily get erect. However, a growing body of research suggests that this strategy may be suboptimal for long-term erectile health, especially when compared to nightly dosing protocols. This is the main reason I am writing this post. 

Several key studies have demonstrated that regular, nightly use of PDE5 inhibitors leads to sustained improvements in erectile function, even after the medication is discontinued. This suggests that these drugs are doing more than just acutely improving erections—they are actively preserving and even restoring erectile tissue health.

Key Studies Supporting Nightly PDE5i Use

1. Long-Term Improvement in Erectile Function Scores

In a randomised controlled trial by Mathers et al., men with mild-to-moderate ED were assigned either fixed low-dose nightly sildenafil (25 mg) or vardenafil (5 mg), or a variable-dose regimen based on nocturnal penile tumescence (NPTR) measurements​. (They were tracking their erections during the night to dial in the dose)

After one year of nightly PDE5i therapy, 64% of men in the fixed-dose group and 75% in the NPTR-guided group had erectile function (EF) scores in the normal range​. Wow!

More impressively, even after stopping the medication for a four-week washout period, 35% of men in the fixed-dose group and 62% in the NPTR-guided group maintained normal erectile function​. They had been cured. 

(Mathers, M. J., Klotz, T., Brandt, A. S., Roth, S., & Sommer, F. (2008). Long‐term treatment of erectile dysfunction with a phosphodiesterase‐5 inhibitor and dose optimization based on nocturnal penile tumescence. BJU International, 101(9), 1129–1134)

2. Persistent Benefits After a Washout Period

Another study by Sommer et al. examined 50 mg nightly sildenafil versus on-demand use over one year, followed by a one-month and six-month washout phase​.

After the first washout phase, 60% of men in the nightly sildenafil group retained normal erectile function, compared to just 8% in the on-demand group​.

Of those who maintained normal erectile function, 95% were still functional six months later, despite no further medication​. They had been cured. 

(Sommer, F., Klotz, T., & Engelmann, U. (2007). Improved spontaneous erectile function in men with mild‐to‐moderate arteriogenic erectile dysfunction treated with a nightly dose of sildenafil for one year: A randomised trial. Asian Journal of Andrology, 9(1), 134–141)

4. Enhanced Endothelial Function and Erectile Response in Animal Models

In a preclinical study by Behr-Roussel et al., rats were given daily sildenafil for eight weeks, and their erectile responses were evaluated​.

Endothelium-dependent relaxations of cavernosal smooth muscle were significantly enhanced, indicating improved endothelial nitric oxide synthase (eNOS) function​.

Additionally, rats that had been on chronic sildenafil therapy responded more strongly to acute sildenafil administration, suggesting a lasting improvement in cavernosal responsiveness​.

Importantly, there was no evidence of tachyphylaxis (tolerance)—a concern sometimes raised with long-term PDE5i use​.(Behr‐Roussel, D., Gorny, D., Mevel, K., Caisey, S., Bernabé, J., Burgess, G., Wayman, C., Alexandre, L., & Giuliano, F. (2005). Chronic sildenafil improves erectile function and endothelium‐dependent cavernosal relaxations in rats: Lack of tachyphylaxis. European Urology, 47(1), 87–91)

Why Does Daily (well, nightly) Dosing Work?

Unlike on-demand use, which simply provides a short-term boost in erectile response, daily PDE5i therapy (taken before sleep) appears to induce lasting structural and biochemical changes in the erectile tissue. The mechanisms behind this include:

Prolonged cGMP Availability → Sustained Vasodilation

PDE5 inhibitors block the breakdown of cyclic guanosine monophosphate (cGMP), allowing prolonged smooth muscle relaxation and vasodilation.

Over time, this repeated exposure to high cGMP levels leads to structural adaptations in the endothelium and smooth muscle, increasing the penis’s baseline ability to achieve and sustain erections​. It’s probably not the cGMP levels themselves, but rather the higher oxygen pressure and the stretching stimulus that does the actual heavy lifting, as we can infer from part 1. 

More Nocturnal Erections → Less Fibrosis, More Smooth Muscle Retention

As established in Part 1, nocturnal erections are a cornerstone for maintaining penile oxygenation and preventing fibrosis.

Regular nightly PDE5i use increases the frequency and quality of nocturnal erections, thereby protecting against cavernosal smooth muscle atrophy and collagen deposition​.

Endothelial Repair and Angiogenesis

PDE5 inhibitors enhance nitric oxide (NO) signaling, which in turn stimulates endothelial repair and the formation of new blood vessels (angiogenesis)​. 

This effect is particularly important for men with endothelial dysfunction (e.g., due to diabetes, hypertension, or ageing), as it can reverse some of the microvascular damage contributing to ED​.

Taken together, these findings suggest that nightly PDE5 inhibitor use is not just a symptomatic treatment—it has the potential to fundamentally restore erectile function by reversing the underlying pathological processes of vasculogenic ED.

Optimising Treatment: The Role of Dose Titration and Individual Response

While the evidence for nightly PDE5i use is compelling, not all men respond equally to the same dosage. In some cases, suboptimal dosing can lead to limited efficacy, while higher doses may cause unnecessary side effects. This is where dose titration and individualised treatment strategies come into play.

The Importance of Dose Adjustments Based on NPTR Measurements

The study by Mathers et al. demonstrated that optimising PDE5i dose based on nocturnal penile tumescence (NPTR) results led to superior outcomes compared to a fixed-dose regimen​. Slightly superior, that is. Let’s not make too much of it. 

In this study, men were given the lowest effective dose that induced full nocturnal erections, determined via NPTR monitoring. 

Those in the dose-adjusted group had higher erectile function scores than those who received a fixed low dose (25 mg sildenafil or 5 mg vardenafil)​. 

Salvaging PDE5i “Non-Responders”

One of the most significant findings from these studies is that some men who initially do not respond well to on-demand PDE5i therapy can become “responders” with nightly dosing. This can be attributed to:

1. Progressive endothelial and smooth muscle improvements with continuous use.

2. More frequent nocturnal erections, leading to structural recovery.

3. Avoidance of performance anxiety effects, which can sometimes hinder the effectiveness of on-demand dosing.

In clinical practice, men who have previously failed on PDE5 inhibitors should not be written off as “non-responders” without first trying a nightly dosing protocol.

Key Takeaways for Optimising Treatment

If you have actual erectile dysfunction, obviously don’t take medical advice from me. I’m just a dude on the internet with no medical degree. Erectile dysfunction with sudden onset can be a sign of really bad underlying diseases, so don’t self-treat with tadalafil without first seeing a urologist or even your general practitioner to get a check-up. 

Start with a low dose and adjust based on response. Many men benefit from as little as 5 mg tadalafil or 25 mg sildenafil nightly. If we add citrulline to this, and some NAC and some supplements to boost glutathione, we should be golden - we are going further than what has been looked at in medical literature. 

If your nocturnal erections do not improve within 2–4 weeks, increase the dose.

Use NPTR monitoring if possible. NPTR-guided dose adjustments have been shown to enhance long-term outcomes​. If NPTR is unavailable, subjective improvements in nocturnal and morning erections can serve as a useful proxy. However, I believe we are generally pretty bad at remembering what happens during the night, and we will mostly only vaguely remember what happened in the last 30 minutes or so. I currently have a FirmTech TechRing that I am evaluating, and will be doing a write-up about it (a review) https://myfirmtech.com/products/the-tech-ring - a kind of “fitbit for the dick” since it records your nocturnal erections and tracks them with a mobile app. I will use it to try and dial in the right dose of tadalafil and citrulline before bed, and also test some other interesting compounds that can tweak nocturnal erections such as Trazodone (works on the serotonin system), a statin (improves endothelial health and NO bioavailability), and some other things as well that my buddy Semtex is recommending me.

On the TSoPE discord, we are discussing a sponsored trial where another NPTR-tracker company (Adam Health) might donate their “Adam Sensor” (https://talktoadam.com/adam-sensor) - I say “we” but it’s really Semtex who is the mastermind here - I’m just happy to tag along, and I can contribute by writing things like this post, for instance.:) 

Many men prematurely quit PDE5 inhibitors due to perceived lack of efficacy. This is sad, because benefits may take several months to fully manifest as structural and vascular changes occur. Remodeling of tissues inside the penis takes time - and it will be slower in humans than in rats, of that I’m sure. 

In the Sommers study I wrote about, they used Sildenafil, which I think was a good choice for a study where you want to look at the effect of nocturnal erections on penile health in isolation. Sildenafil has a rapid onset and short half-life, so most of it will be flushed from the system by mid morning for sure if you take it before bed. However, I think we should be using tadalafil instead of sildenafil for three reasons: 1. It will be more active toward the end of the night, where you will have the most nocturnal erections anyway. 

1. It tends to have less side effects like nasal congestion, dry eyes, changes in vision due to effects on internal eye pressure, headaches, blushing, etc. 

2. It will be active the whole day after, which is neat for spontaneous sex or for PE sessions.  

The drawback, of course, is that it’s more expensive. Cialis is my main expense where PE is concerned. 

Other things to consider: 

Sleep Optimisation

Nocturnal erections occur primarily during REM sleep, meaning poor sleep quality can directly reduce their frequency.

Best practices for sleep hygiene include:

-Consistent sleep schedule (going to bed and waking up at the same time each day).

-Avoiding blue light exposure from screens at night.

-Managing stress and reducing caffeine intake in the evening.

-Huberman says sunlight exposure in the morning is important for the circadian rhythm, so maybe do that as well. 

Milking, RIP and hypoxia-reperfusion

I previously mentioned that I will be doing some form of rapid interval pumping or “milking” for the rest of my life, since I regard them as probably the best thing you could possibly do to maintain erectile health, apart from having a healthy lifestyle of course. 

With an auto-Pump that can do rapid intervals, getting these sessions done is a breeze. Set it and forget it. Cycling that oxygen-rich blood in and out to provide nutrients, antioxidants, while at the same time getting a cyclic stretching stimulus to the endothelial and smooth muscle cells… if you have paid attention, you will realize that milking and RIP mimic what nocturnal erections do. 

In this post I look closer at how hypoxia can be used strategically: https://www.reddit.com/r/TheScienceOfPE/comments/1i0lnsg/the_role_of_vegf_and_strategic_ischemia_in/ 

I will not repeat here what I said in that post, I will only reiterate the main point I make: Ischemia and Reperfusion Dynamics research shows that ischemia can have a biphasic effect: short-duration ischemia increases VEGF expression and promotes angiogenesis, while prolonged ischemia suppresses VEGF and elevates fibrosis markers like TGF-beta1. Remote ischemic preconditioning (RIPC), which involves cycles of brief ischemia followed by reperfusion, has been shown to reduce pro-inflammatory and pro-fibrotic markers while enhancing vascular health. (Damn Karl, do you have to use so much bold typeface? Yup, because all of that was important, lol.)

Part 3 - Why Nocturnal Erections Matter for Penis Enlargement

Some of the activities we do in PE cause a pro-fibrotic stimulus. Vacuum hanging or compression hanging (which includes extending) done in a manner where your glans gets cold and purple: Hypoxic low-flow state! Extending so your penis gets super thin: Hypoxic low-flow state. Clamping for more than 10 minutes: slightly low-flow state with mild hypoxia. All of these will to some degree up-regulate transforming growth factor-beta 1. We have good reasons to want to counteract that with RIP + Milking + Nocturnals-boosting!

But perhaps the most important point that pertains to PE is that we are increasing the volume of our penises, and that means the cavernosal sinusoids need to grow too, and maintain their elasticity. So we want to stimulate VEGF and suppress TGF-β1 expression to allow this tissue to grow and be in good health so we “fill the sausage”. This helps us close the gap between bpel and bpsfl, and it helps us maintain a good veno-occlusive function when the tunica is growing and requires the CC to grow in order to be able to seal off the subtunical venules. 

And finally we have the aspect of “shape retention”. By doing PE work in the evening, you cause your tunica to become expanded, and the more you can allow it to stay in that expanded state, the more likely it is that it will retain the ability to be that size - i.e. it aids the conversion of temp-gains to perma-gains. I have a longer article on shape retention on my blog, and while I don’t think it’s the be-all, end-all of PE, I believe it will probably affect our gain rate to an extent. If I had unlimited privacy and a supply of decently effective non-addictive painkillers I would be injecting my D with PGE1 to induce 4-hour priapisms several times per week for shape retention purposes (and because PGE1 has actually been shown to be anti-fibrotic to the endothelial tissue).

Some final words

There are things you should do FIRST, before jumping on a protocol of milking, cialis and citrulline. 

If you have metabolic syndrome with mitochondrial dysfunction, dysregulation of appetite due to leptin resistance, and systemic inflammation due to chronically elevated IL-6 and TNF-alpha, resulting in conditions like central adiposity with intrahepatic and visceral fat accumulation, insulin resistance, diabetes type 2, ischemic heart disease, hypertension, obesity, anxiety and depressive disorders, etc, you should 1000% do something about that. I can give detailed instructions, but the gist is to exercise and eat a low-glycaemic diet where you exclude fructose, and to do some occasional water fasting for AMPK / mTOR balancing and stimulation of mitogenesis. GLP1 and GIP receptor agonists such as semaglutide and tirzepatide can be of assistance too, as can a stack of supplements to suppress inflammation and increase mitochondrial function by supporting glutathione function. Note that I didn’t tell you to “just lose weight you lazy bastard” as some influencers do. That’s unhelpful. Weight loss happens as a positive side effect of getting metabolically healthy, not the other way around. That is a key insight I wish more people had.

If you smoke or drink alcohol, fucking quit today ffs! Fine, indulge a few times per year—but if you have a habit, quit it. 

If you have a sedentary lifestyle where you mostly sit at the computer all day and night, this is poor for vascular function and increases inflammatory markers. Take daily walks, most days of the week. Doesn’t have to be more advanced. 

If something is good for your overall health, it also tends to be good for your erectile health, it really is that simple. 

When you are doing something about all of these things to improve your dick, you have my permission to start with the cialis-citrulline-milking protocol. :)

I apologise for writing such a long post. I write mostly to organise my own thoughts and as a part of doing my own research, and as a result I tend to be long-winded. I probably made a mistake or two somewhere in this post, and if you help me spot them I would be grateful.

This took me about 24 hours to write, so please leave an upvote and a comment if you found it useful, to help the algorithm pick it up so that more people see it. :)

Karl — over and out.

Some further reading

(thank you Semtex for the links!)  https://www.medscape.com/viewarticle/477592 “Long-term Nightly Sildenafil Promotes Normal Erectile Function”

https://f1000research.com/articles/14-142 “Correlation between Erectile Function Assessment through International Index of Erectile Function Score and Nocturnal Penile Tumescence and Rigidity Measurements in Men with Erectile Dysfunction”

https://www.sciencedirect.com/science/article/abs/pii/S0302283804004646 

“Chronic Sildenafil Improves Erectile Function and Endothelium-dependent Cavernosal Relaxations in Rats: Lack of Tachyphylaxis”