Erections are a function of the change of balance between constriction and relaxation. Both can have a dysfunction, alone or together. Not just the relaxation part of the equation which PDE5 inhibitors assist with.
You could also be developing issues with atherosclerosis, which will impede blood flow into the penis. An early warning sign of what might be occurring in vital organs such as the heart. This begins with endothelial dysfunction in the corpus cavernosum which will lower NO availability.
PDE5 inhibitors will help initially with this but as the condition worsens they will become less effective. They become less effective because the generation of NO is a few steps back before the point whereby PDE5 inhibitors perform their action. PDE5 inhibitors will do nothing at all if there is little to no NO. The pathway becomes more and more dysfunctional and progresses to plaque build-up and fibrosis in the penis and much further down the track, heart disease. High blood pressure contributes to endothelial dysfunction as does diabetes. Anyone experiencing ED at your age needs to be checked out for early signs of the above IMO.
Oxidative stress is something that occurs due to excessive stress on the body and unfortunately, ageing. You did mention you are a powerlifter. Are you over-training? What is your diet like? Do you do any cardiovascular exercise to help prevent endothelial dysfunction and heart disease? Have you ever done anabolic steroids? High levels of weight training coupled with anabolic steroids can lead to oxidative stress.
Research has found that oxidative stress can promote sympathetic hyperactivity and endothelial dysfunction, which means not only is the vasodilation part of the erection process compromised, but also the smooth muscle in the penis and arteries are more likely to stay constricted due to excess norepinephrine generated by the sympathetic nerves within the penis itself.
If you can get a good erection while watching “porn” (you didn’t mention if PDE5i was needed for this), your ED could be more related to a psychogenic cause. With all the research I have done in the past years, psychogenic ED appears to be closely related to a hyper sensitivity to the contractile mechanism of norepinephrine in the penis. Given your age, as I have already mentioned there could be other causal factors or one which generates more than one dysfunction for example; the inability of the penis to trap blood effectively and the inability for it to relax sufficiently to allow more blood to enter (not necessarily your issues).
I think if one was to watch erotic material on the odd occasion it would do no harm. However, I think if it becomes an addictive behaviour, (like any addictive behaviour) then it could be a problem, not physiologically, but it may create a possible psychological dependence whereby the dopamine release is addictive. All things in moderation.
I am sceptical of the theories of “dopamine burnout” as there is no real scientific evidence of this. I think what is happening is a result of over exposure, it becomes so familiar and regular that the dopamine release we once got from it becomes muted, and thus commonplace. The brain is very adept at limiting how much of a dopamine release we experience for survival reasons. As you mention you watch “tons of porn”, this does suggest it may be in excess. If so, it might be a good idea to refrain for a reasonable period of time. let your mind re-sensitise to the sexual act. Put the “porn” away for 6 months.
If you can get and keep an erection whilst watching “porn”, two things may be happening more effectively than when you try and have sex with someone. Firstly, there is no one there to judge you, no one to perform for but yourself. As you are in a relaxed state the tipping point is in your favour of being able to have an erection even though you may have an increased sensitivity to the contractile forces of norepinephrine. It just gets you over the line, so to speak. Combine this with the high stimulation that pornography can bring to the senses, levels of NO may be enhanced which further tip the balance of power in favour of smooth muscle relaxation in the corpus cavernosum and blood can flow readily to fill its expanding spaces. Conversely, when you attempt to have sex with someone the tipping point of power of one or even both may be more in favour of the opposite as the higher sensitivity to norepinephrine and possibly even a slightly lower level of excitement allows the contractile machinery to easily take over. A viscous cycle most likely then develops as the subject becomes even more anxious about the failure of not being erect and the body’s sympathetic nervous system plunges further into flight and fight mode. This IMO can take time to subside.
If you did not have the heightened sensitivity to norepinephrine in the penis such as in the case of a normal young male, the requirement for being very relaxed and the high visual stimulation of erotic material would not be needed for an erection to occur. In other words the balance of power is more even and erections occur without too much inhibition from norepinephrine. As soon as some form of stimulation occurs be it mental of tactile, the NO pathway can easily take over and supress the sympathetic pathway as it should.
I think in the earlier stages of sympathetic hyperactivity, a PDE5 inhibitor may be sufficient to overcome the problem, as the enhancement of the effect of NO will be enough to suppress sympathetic activity sufficiently. As the person ages, this hyperactivity appears to increase and cannot be mitigated by enhancing the levels of cGMP alone. Also as I mentioned above levels of NO can slowly decrease for a multitude of reasons as we age, which lessens the positive effect of a PDE5 inhibitor. Perhaps not so much at your age. However, there can be a definite deterioration in cellular function at the age of 40 compared to the age of 20, which can be exacerbated by lifestyle.
How do we combat this? The bad news is there is nothing available in the US, Australia and the UK, legally and specifically to combat this form of ED other than Trimix. One of the three compounds in Trimix (Phentolamine) blocks to an extent, the sympathetic pathway. The other two assist with vasodilation. Because it is injected into the penis, it is concentrated in the area where it is needed and can block those receptors in the penis specifically rather than systemically.
Oral A1 selective adrenergic receptor blockers are available, but they are approved for use primarily with LUTS and BPH. Some urologists are recognising the above condition in younger men with ED and are prescribing these medications to help treat what they term as “hypertonic cavernous smooth muscle”, in other words sympathetic hyperactivity. This apparently works for some men an others not so. A receptor blocker which blocks both A1 and A2 adrenergic receptors (non-selective) might work better for others. The oral ED drug developed for this was called Vasomax, which is Phentolamine mesylate (PM). It did not get approval in the countries I mentioned above. I think it appeared about the same time as PDE5 inhibitors, and may have been pushed to the side by its much bigger brother; Viagra.
There was also a study done with PM on rats in high doses and there was evidence of carcinogenic activity in the very high dose range. This in combination with the competition with Viagra, may have halted its approval. I think other members on this forum know more on this issue. It is currently prescribed in some countries, but I do not have information as to the possible carcinogenic implications it has had in those countries, if any. There are studies also showing its effectiveness and safety in human trials. It is approved for use as an injection directly into the penis.
Another member on this forum has discussed his success with PM, for psychogenic ED, to help combat this condition for the reasons mentioned above, with success. He knows far more than I do about this medication. Do a search for posts by Flavio.
The aetiology of erectile dysfunction for most evolves over time. In other words, what causes it doesn’t stay constant. The ageing process itself causes other dysfunctions to appear, and what might have started out as “psychogenic” ends up being a number of processes that have become compromised.
I hope the above helps give you a better understanding of what may and I repeat may, be affecting your erectile function.
Much of the above is quite simplified and still considered research and hypothesis. There are of course other processes involved with the constriction and relaxation events in the Penis such as the RHO-Kinase pathway, which is quite complex and currently the subject of much research with regard to ED.
It appears that the human penis is not as robust in design as perhaps other organs in our bodies, possibly because it’s not a vital organ and mother nature prefers fresh new genetic material from young males. The male is in his peak during his teens and early twenties. After that it’s all downhill!
. I would like to see that study that you mentioned on men who did not have ED and used PDE5 inhibitors in large amounts, causing ED. If you find the link please post it.
