ED issues with TRT absolutely lost and local doctors dont seem to have any answers.

[Spartan1985]

I don't think it makes sense in using HCG if you're having Estradiol issues, as HCG is known to increase it to a good degree. You should find what works for by using the least amount of substances, adding other substances should be done after you stabilized the protocol you currently run. Also HCG doesn't need to be injected everyday, 2-3x a week is fine, because of its half life. 75 IU/day (525 IU/week) also isn't a too high of a dose, I'd say the typical weekly dose is 500-1000 IU.
Test P is great for many reasons and one of them is quick symptom relief and saturation, you should have stable blood levels after 1 week. This means you can very quickly adjust your protocol, which is great if you're experimenting on how your body works and reacts. However I'd still do regular blood tests to see where you stand with some dose. While it's not bad to try out a lower dose, the reality is that if your trough is at 500 with 120mg/week, then with 84mg/week your dose might be too low and you'd feel bad. Nothing wrong with trying it out anyway, but having some data at least explains what's going on and sets some expectations. Personally I did regular blood tests during my experimentation, but I mostly tested just total T and E2, as this was enough to tell me what's going on, and to keep the costs of tests as low as possible.

If your interested here is my own thread about my experimentation with a bunch of updates: Test P improved TRT, libido still at 0 – what next?

Yeah I’d agree with the less substances the better for both monitoring and health reasons. I haven’t had great results with hcg and feel it’s added to the problem as the best stability has been found without it, that’s why I was interested in why Rotngun was suggesting add that dose at the moment. Just out of interest of learning as not in any position of understanding to doubt his input. I’m happy with your previous suggestion it makes sense so Prop ordered, should be here this week. Last E jag was Thursday so will start daily delt shots Friday onwards at the dose you suggested and see how things settle from there. Can prop be taken via insulin needle subQ as that would be a bit easier to deal with if possible due to no experience of self administered injections other than subQ hcg or pt141? Thanks I’ll have a read through that just now. Really appreciate everyone’s response it’s been good even getting to be able to talk about this stuff. Only know 1 or 2 guys at the gym on TRT and both say they feel 18 again always horny and full of energy with superb erection quality which probably makes my experience seem worse

 

[ziegen]

Yeah I’d agree with the less substances the better for both monitoring and health reasons. I haven’t had great results with hcg and feel it’s added to the problem as the best stability has been found without it, that’s why I was interested in why Rotngun was suggesting add that dose at the moment. Just out of interest of learning as not in any position of understanding to doubt his input. I’m happy with your previous suggestion it makes sense so Prop ordered, should be here this week. Last E jag was Thursday so will start daily delt shots Friday onwards at the dose you suggested and see how things settle from there. Can prop be taken via insulin needle subQ as that would be a bit easier to deal with if possible due to no experience of self administered injections other than subQ hcg or pt141? Thanks I’ll have a read through that just now. Really appreciate everyone’s response it’s been good even getting to be able to talk about this stuff. Only know 1 or 2 guys at the gym on TRT and both say they feel 18 again always horny and full of energy with superb erection quality which probably makes my experience seem worse

All of these substances can be injected with an insulin needle, I've been doing so since the beginning of TRT. Yes, you can do SubQ, I personally inject SubQ and prefer it, good spots are the belly, love handles and ventroglutes. Ventroglutes are also a good spot for IM injections and it's far easier to pin here than in delts. The only thing with SubQ is that some people seem to have a worse response to it compared to IM, maybe those who have higher body fat % (maybe above 20%)? I have tried IM and SubQ and did blood tests for both methods, the symptom relief and bloods have been the same, so for me there is no difference in terms of "performance".

Yeah for most people TRT is far easier and seem to have better symptom relief. I know some guys on TRT and many that abuse steroids and I haven't met a single person that would have libido issues to such an extreme degree as me. Many have been surprised that it's even possible. The only ones that had libido issues have gone to extreme doses and a lot of extra substances that fucked with their system. I don't think you're in a bad position, you more or less know what's wrong, you just need a systematic approach to your treatment and start low and slow.

 

[ziegen]

Might want to tell the guy to tread lightly when it comes to driving up your FT too high off the hop!

Better yet the complexity involved when it comes to libido and erectile function!

Everyone so caught up on T, DHT and estradiol LMFAO!

Much more involved than just having healthy hormones!

Test P improved TRT, libido still at 0 – what next?

I've been on TRT for roughly 3.5 years now, with very limited results. I started and kept using Test E most of this time. In the honeymoon phase I had great symptom relief, however after 3 months almost all of those symptoms returned, I only felt better emotionally and mentally. Honestly I was...

www.excelmale.com

Truth About Testosterone and Your Libido

https://www.yahoo.com/lifestyle/truth-testosterone-libido-185000725.html?soc_src=social-sh&soc_trk=tw&tsrc=twtr As an expert on andrology and sexual dysfunctions, urologist Andrew Y. Sun, M.D., sees plenty of patients who’re struggling with low libido. And most are pretty sure they already...

www.excelmale.com

*The male sexual response cycle is complex and the exact role of testosterone in mediating libido, arousal, erection, ejaculation, and orgasm is multifactorial

*This hormone isn’t the only biological factor with clear, substantial power over our libidos

Testosterone + Men's Sexual Health

Dr. Dubin is a fellowship-trained urologist and andrologist focusing on men’s health. He cares for men with fertility problems, sexual issues (erectile dysfunction, premature ejaculation, delayed ejaculation, etc.), Peyronie’s disease, low testosterone, testicular pain and other problems...

www.excelmale.com

Much more to the story when it comes to testosterones impact on libido/erectile function!


*Again having a healthy FT is only one piece of the puzzle as libido let alone ED are multifactorial.

*Getting quality sleep, minimizing stress (physical/mental), following a healthy diet, exercising/staying active, improving overall vascular health will have a far bigger impact than jacking up your trough FT!

*Have realistic expectations especially when it comes to libido and erectile function!

OP had a problem with his TRT protocol, he had results, but were inconsistent due to the "crashes" he experienced. I provided some information and a plan to hopefully help him dial in. I didn't see a need to go in dept about lifestyle or thyroid hormones or anything similar as I think someone on TRT should already realize these things, especially if he was dealing with decent doctors, so I considered it off topic. Of course if he hasn't checked these things or got them in order, then it would make sense to do so.

Personally I did regular blood tests during my experimentation, but I mostly tested just total T and E2, as this was enough to tell me what's going on, and to keep the costs of tests as low as possible.

TT means nothing without knowing where your FT level sits!

Again as I have been preaching on the forum over the years although TT is important to know FT is what truly matters as it is the active unbound fraction of T responsible for the positive effects!

Throw in the RBCs, hemoglobin and hematocrit too which are also critical blood markers that one needs to know when using exogenous T!

It was stressed in my reply to you how absurd your trough FT was on that whopping daily dose of TP you were injecting!

As you should very well know TP has more active T/mg.

Again to put this in perspective.

We can nitpick here on the approx free equivalents but you get the point!

25 mg TP (175 mg/week) is a whopping amount of active T (minus the ester).

175 mg TP (145.25 mg active T)/week would be the equivalent of banging 207.5 mg TC (145.25 mg active T)/week.

This gets even more nuttier when you think about the daily production of a healthy young male which would be 5-7 mg T, 10 mg T daily top f**king end to boot which would be 70 mg T/week!

Your were banging 145.25 mg T/week or better yet 20.75 mg T daily!

Most men on TTh are injecting 100-200 mg TC or TE/week whether once weekly, twice-weekly (every 3.5 days), M/W/F, EOD or daily.

The majority of men can easily hit a healthy let alone high or in some cases absurdly high trough FT injecting 100-150 mg T/week especially when split into more frequent injections.

Yes there are outliers who may need the higher-end weekly dose 200 mg T/week but it is far from common as in RARE!

Such dose would be overkill for the majority.

Your trough FT was is in the 30s ng/dL which is absurdly high!

Again this is your trough (lowest point) 24 hrs post-injection as you were injecting a whopping 25 mg TP daily.

Again show me a healthy young male with low/lowish SHBG hitting a TT 1000+ ng/dL.....such does not exist!

Top it off that your peak TT/FT would have been sky-high due to the PK of TP.

You were clearly overmedicated here!

Test P improved TRT, libido still at 0 – what next?

I've been on TRT for roughly 3.5 years now, with very limited results. I started and kept using Test E most of this time. In the honeymoon phase I had great symptom relief, however after 3 months almost all of those symptoms returned, I only felt better emotionally and mentally. Honestly I was...

www.excelmale.com

OP was already using higher doses than what I recommended, and he has the blood tests done, so I think it was a good dose and protocol adjustment recommendation. I know that full blood panels are better, and I personally have quite many, but after a few you already see a pattern. Someone with low SHBG is not going to magically have high SHBG suddenly, so you can make an accurate prediction on where things stand. In my post I just inserted a snippet of my blood panel, as the rest wasn't relevant, it was fine. For my experimentation my point was to get a feel where I stand and how I feel, and it was not economical or made sense, in my opinion, to do a comprehensive blood panel every time. I realize what I was doing, I wanted to try a higher doses for a while to see if anything would improve/change, but it didn't so I started lowering it soon after, and started trying lower doses.

In any case this is a bit off topic as it's more about what I was doing back then, than what OP is facing and doing now.

 

[Spartan1985]

All of these substances can be injected with an insulin needle, I've been doing so since the beginning of TRT. Yes, you can do SubQ, I personally inject SubQ and prefer it, good spots are the belly, love handles and ventroglutes. Ventroglutes are also a good spot for IM injections and it's far easier to pin here than in delts. The only thing with SubQ is that some people seem to have a worse response to it compared to IM, maybe those who have higher body fat % (maybe above 20%)? I have tried IM and SubQ and did blood tests for both methods, the symptom relief and bloods have been the same, so for me there is no difference in terms of "performance".

Yeah for most people TRT is far easier and seem to have better symptom relief. I know some guys on TRT and many that abuse steroids and I haven't met a single person that would have libido issues to such an extreme degree as me. Many have been surprised that it's even possible. The only ones that had libido issues have gone to extreme doses and a lot of extra substances that fucked with their system. I don't think you're in a bad position, you more or less know what's wrong, you just need a systematic approach to your treatment and start low and slow.

Think I’ll go with subq for daily injections as it’s what I’m most comfortable with self administering. I read through your thread, you’ve certainly had a turbulent journey and sad to read you’re still not any closer to an answer on the libido issue. The technical detail of some of the responses on your thread are incredible, the understanding some guys have of this process is really impressive. I tried pt141 also, it helped for ED but the sides were terrible. Didn’t do anything for my libido at all though. Had limited success with caber during PCT phases of my steroid using years though and it did give a lift but it’s extremely powerful and even half a tablet once was quite a lift. Tapered off quickly and soon had no affect though for whatever reason. If dopamine is a possible cause there are some peptides that can assist with that, only know that as I’ve been told my ED issues may be dopamine related and to explore that option. Just want to get the TRT protocol accurate if possible as urologist is adamant my issue is hormonal. Really hope you get a result soon. I like your systematic approach though and will be implementing that style a lot in the coming months. Guess until now I’ve been following the TRT docs advice pretty blindly as to be honest I get lost in the science of it all.

 

[RotnGun]

Seems logical, can I ask why you suggest such a high dosage over the week of hcg? (Compared to what I’ve been prescribed over the last year) I’m going to try what Ziegen recommended with slightly higher Prop dose with no hcg at all to start as so far the issues seem to come from E2 so from my limited understanding his protocol should have less e2 spike and see if I need to adapt from there. If I don’t get any relief from symptoms with that I’ll try lower dose Prop with some hcg and see how I react to that. Do you defo think 75iu per day is needed? I have no fertility requirements as already have 3 kids and honestly couldn’t cope with a 4th lol

It really depends on how you react to TRT. I have to use the HCG to avoid testicular atrophy and achyness. Plus, HCG helps a little bit to make my body produce some testosterone to add in addition to my 10mg of test cyp per day. The large majority of guys will experience testicular atrophy and achyness eventually at some point in their lives. 75iu of HCG per day is not much, as it only equals to 525iu per week. To say the truth, Im very likely injecting 70iu per day because there is an air bubble in my syringe as well as a little liquid left behind after injecting. But thats a trivial matter though. Its known that 500iu of HCG is the minimal amount needed to avoid testicular atrophy and testicular achyness. Obviously, some guys may need more than that to prevent those side effects. But overall, 500iu of HCG per week should really not affect estogen values that much for most guys. The higher the dose you go, then the more likely you will have estrogen issues. It seems to happen to guys when they go over 750iu of HCG per week or inject a whopping dose of 300iu every 3 days. I take 75iu daily because the half life of HCG is 48 hours and 75iu daily will last a long time in my body

 

[Spartan1985]

It really depends on how you react to TRT. I have to use the HCG to avoid testicular atrophy and achyness. Plus, HCG helps a little bit to make my body produce some testosterone to add in addition to my 10mg of test cyp per day. The large majority of guys will experience testicular atrophy and achyness eventually at some point in their lives. 75iu of HCG per day is not much, as it only equals to 525iu per week. To say the truth, Im very likely injecting 70iu per day because there is an air bubble in my syringe as well as a little liquid left behind after injecting. But thats a trivial matter though. Its known that 500iu of HCG is the minimal amount needed to avoid testicular atrophy and testicular achyness. Obviously, some guys may need more than that to prevent those side effects. But overall, 500iu of HCG per week should really not affect estogen values that much for most guys. The higher the dose you go, then the more likely you will have estrogen issues. It seems to happen to guys when they go over 750iu of HCG per week or inject a whopping dose of 300iu every 3 days. I take 75iu daily because the half life of HCG is 48 hours and 75iu daily will last a long time in my body

Testicular atrophy has always been an issue since starting and the doses of hcg to date haven’t managed to rectify that. It has defo led to additional complications with oestrogen though as found things improved in some ways since dropping it. Haven’t tried daily smaller doses though to be fair. Wonder if the smaller infrequent doses have been why it’s been unsuccessful so far. As Ziegen said in his last reply low and slow back to basics would be best approach but if not getting much of a result on the 17.5mg daily SubQ will drop dose and add the hcg daily and monitor how that works over 3-4weeks.

 

[ziegen]

Think I’ll go with subq for daily injections as it’s what I’m most comfortable with self administering. I read through your thread, you’ve certainly had a turbulent journey and sad to read you’re still not any closer to an answer on the libido issue. The technical detail of some of the responses on your thread are incredible, the understanding some guys have of this process is really impressive. I tried pt141 also, it helped for ED but the sides were terrible. Didn’t do anything for my libido at all though. Had limited success with caber during PCT phases of my steroid using years though and it did give a lift but it’s extremely powerful and even half a tablet once was quite a lift. Tapered off quickly and soon had no affect though for whatever reason. If dopamine is a possible cause there are some peptides that can assist with that, only know that as I’ve been told my ED issues may be dopamine related and to explore that option. Just want to get the TRT protocol accurate if possible as urologist is adamant my issue is hormonal. Really hope you get a result soon. I like your systematic approach though and will be implementing that style a lot in the coming months. Guess until now I’ve been following the TRT docs advice pretty blindly as to be honest I get lost in the science of it all.

Well I gained all this knowledge, because I had no choice, but to go deeper. Unfortunately I have fixed my hormones now to a high degree and have massive symptom relief, other than libido, so it works quite well. Overall there is no pride or ego in this knowledge, I'd much rather have great success immediately upon starting TRT and forget about all this, but what can you do. In the end you can feel limited results and either accept this state or start experimenting more to find a solution. Experiment or don't, you won't feel amazing either way until you find something, so might as well do something that will hopefully deal with your issues in the future. Doing it systematically and getting regularly tested just ensures that you have the best possible approach and data. Considering you mentioned that you have a great symptom relief for weeks and then you suddenly crash, I think it's safe to assume that it's hormonal. In my case my libido has been at a constant 0, regardless of what I've tried, so I think the problem is something additional to hormones.

Testicular atrophy has always been an issue since starting and the doses of hcg to date haven’t managed to rectify that. It has defo led to additional complications with oestrogen though as found things improved in some ways since dropping it. Haven’t tried daily smaller doses though to be fair. Wonder if the smaller infrequent doses have been why it’s been unsuccessful so far. As Ziegen said in his last reply low and slow back to basics would be best approach but if not getting much of a result on the 17.5mg daily SubQ will drop dose and add the hcg daily and monitor how that works over 3-4weeks.

Well it also depends on how long you've been doing TRT before adding HCG. So how much atrophy you have before HCG. I was on TRT for 2 years with Test E before adding HCG and 500 IU/week wasn't enough to do anything, because I was already suppressed for so long. In this case people take much higher doses to kick start their system and then reduce the dose to maintain. I did 3000 IU/week split into 3 doses for 1.5 months to get my testicles back to 100%, then I did 600 IU/week split into 2 doses to maintain. Soon after switching to Test P I also dropped HCG due to traveling and I only have minor atrophy compared to a longer ester. I'd say on Test P I only lost about 15-20% of the size, and I have no aching (huge plus), meanwhile on Test E I lost 50-60%. Constant levels of hormones and higher doses suppress a lot more.

 

[Spartan1985]

Well I gained all this knowledge, because I had no choice, but to go deeper. Unfortunately I have fixed my hormones now to a high degree and have massive symptom relief, other than libido, so it works quite well. Overall there is no pride or ego in this knowledge, I'd much rather have great success immediately upon starting TRT and forget about all this, but what can you do. In the end you can feel limited results and either accept this state or start experimenting more to find a solution. Experiment or don't, you won't feel amazing either way until you find something, so might as well do something that will hopefully deal with your issues in the future. Doing it systematically and getting regularly tested just ensures that you have the best possible approach and data. Considering you mentioned that you have a great symptom relief for weeks and then you suddenly crash, I think it's safe to assume that it's hormonal. In my case my libido has been at a constant 0, regardless of what I've tried, so I think the problem is something additional to hormones.


Well it also depends on how long you've been doing TRT before adding HCG. So how much atrophy you have before HCG. I was on TRT for 2 years with Test E before adding HCG and 500 IU/week wasn't enough to do anything, because I was already suppressed for so long. In this case people take much higher doses to kick start their system and then reduce the dose to maintain. I did 3000 IU/week split into 3 doses for 1.5 months to get my testicles back to 100%, then I did 600 IU/week split into 2 doses to maintain. Soon after switching to Test P I also dropped HCG due to traveling and I only have minor atrophy compared to a longer ester. I'd say on Test P I only lost about 15-20% of the size, and I have no aching (huge plus), meanwhile on Test E I lost 50-60%. Constant levels of hormones and higher doses suppress a lot more.

That makes a lot of sense. Weirdly I had hcg from the first prescription but as I started in what’s probably a fairly unusual position having gone from a long steroid cycle to letting it crash to TRT it may have been originally too low going by what you are saying there. Often wonder whether the first TRT doc was right in prescribing TRT given my situation or whether a long PCT would have been a better choice at that point. Suppose I won’t really get an answer to that at this stage so kinda a moot point. I feel happier knowing I’m not the only one to have various issues over a long period trying to dial in the right protocol and feel a little more hopeful about things with the approach you have suggested which makes a lot of sense.

 

[Spartan1985]

Personally I did regular blood tests during my experimentation, but I mostly tested just total T and E2, as this was enough to tell me what's going on, and to keep the costs of tests as low as possible.

TT means nothing without knowing where your FT level sits!

Again as I have been preaching on the forum over the years although TT is important to know FT is what truly matters as it is the active unbound fraction of T responsible for the positive effects!

Throw in the RBCs, hemoglobin and hematocrit too which are also critical blood markers that one needs to know when using exogenous T!

It was stressed in my reply to you how absurd your trough FT was on that whopping daily dose of TP you were injecting!

As you should very well know TP has more active T/mg.

Again to put this in perspective.

We can nitpick here on the approx free equivalents but you get the point!

25 mg TP (175 mg/week) is a whopping amount of active T (minus the ester).

175 mg TP (145.25 mg active T)/week would be the equivalent of banging 207.5 mg TC (145.25 mg active T)/week.

This gets even more nuttier when you think about the daily production of a healthy young male which would be 5-7 mg T, 10 mg T daily top f**king end to boot which would be 70 mg T/week!

Your were banging 145.25 mg T/week or better yet 20.75 mg T daily!

Most men on TTh are injecting 100-200 mg TC or TE/week whether once weekly, twice-weekly (every 3.5 days), M/W/F, EOD or daily.

The majority of men can easily hit a healthy let alone high or in some cases absurdly high trough FT injecting 100-150 mg T/week especially when split into more frequent injections.

Yes there are outliers who may need the higher-end weekly dose 200 mg T/week but it is far from common as in RARE!

Such dose would be overkill for the majority.

Your trough FT was is in the 30s ng/dL which is absurdly high!

Again this is your trough (lowest point) 24 hrs post-injection as you were injecting a whopping 25 mg TP daily.

Again show me a healthy young male with low/lowish SHBG hitting a TT 1000+ ng/dL.....such does not exist!

Top it off that your peak TT/FT would have been sky-high due to the PK of TP.

You were clearly overmedicated here!

Test P improved TRT, libido still at 0 – what next?

I've been on TRT for roughly 3.5 years now, with very limited results. I started and kept using Test E most of this time. In the honeymoon phase I had great symptom relief, however after 3 months almost all of those symptoms returned, I only felt better emotionally and mentally. Honestly I was...

www.excelmale.com

Hi madman, your knowledge seems mega detailed and reads very well. I appreciate the complexity of ED and cannot claim to have the knowledge required to try and rectify it unfortunately. Is there any other biomarkers in my blood results I should monitor/look at that may hold clues to what underlying issues may be adding to it or indeed causing it? Part of my frustration to date has been that I’ve been at low test, high test and everything in between plus the same with E2 and while some things certainly seem to add to it especially E2 issues there always is something that affects erectile quality and literally cannot remember my last morning erection. I have been told to test nitrates etc so have a kit coming shortly with nitric oxide boosters to see if that helps. I’m not 100% convinced the answer to that problem is fully in TRT but feel it would make the best sense to either get a balanced protocol that’s working to rule it out or give up and try restart my system to whatever degree it restarts given the level of shutdown it’s been under over the years. Any input greatly appreciated. You mentioned heamocrat levels, I was told before some people are susceptible to even moderately high levels as it’s relative to blood vessel size however the NHS endocrinologist wouldn’t entertain a discussion on that front

 

[madman]

Hi madman, your knowledge seems mega detailed and reads very well. I appreciate the complexity of ED and cannot claim to have the knowledge required to try and rectify it unfortunately. Is there any other biomarkers in my blood results I should monitor/look at that may hold clues to what underlying issues may be adding to it or indeed causing it? Part of my frustration to date has been that I’ve been at low test, high test and everything in between plus the same with E2 and while some things certainly seem to add to it especially E2 issues there always is something that affects erectile quality and literally cannot remember my last morning erection. I have been told to test nitrates etc so have a kit coming shortly with nitric oxide boosters to see if that helps. I’m not 100% convinced the answer to that problem is fully in TRT but feel it would make the best sense to either get a balanced protocol that’s working to rule it out or give up and try restart my system to whatever degree it restarts given the level of shutdown it’s been under over the years. Any input greatly appreciated. You mentioned heamocrat levels, I was told before some people are susceptible to even moderately high levels as it’s relative to blood vessel size however the NHS endocrinologist wouldn’t entertain a discussion on that front

When it comes to the hormonal aspect having healthy FT, DHT and estradiol levels are critical!

Low levels of any of these hormones would have a negative impact on libido/erectile function.

One does not need high FT let alone DHT in order to have a healthy libido/erectile function.

It's myth that high T will have one running around with a raging libido and titanium erections to boot!

When it comes to using exogenous T having too high a FT especially steady-state can be just as bad in many ways as having too low a FT level especially when it comes to libido and erectile function.

Skewed T:E ration can have a negative impact.

Dysfunction thyroid/adrenals can have a negative impact on libido/erectile function.

Elevated prolactin can have a negative impact on libido/erections.

* Hyperprolactinemia results in reproductive as well as sexual dysfunction. Symptoms associated with hyperprolactinemia include loss of libido, ED, galactorrhea, gynecomastia, and infertility. These symptoms typically occur only at severely elevated levels (>35 ng/mL or 735 mU/L).76

High blood pressure, hyperlipidemia and high blood sugar can damage blood vessels/nerves.

Adrenaline is a libido/EF killer!

* Adrenalin.....anti-erection chemical!

As I stated in a previous thread.

Libido starts in the brain.

Neurotransmitters have a big impact especially dopamine.

There is a fine balance here when it comes to the dopamine system!

This is key here..... dopamine circuits are powerfully regulated by androgens!

Hammering the shit out of your dopamine is the last thing you want to do.

Anything that lowers libido can lead to ED if the drive is absent!

Even then for the majority of older men ED is vasculogenic!

By the time one hits 40 many men will experience some degree of ED (mild, moderate, severe) due to vascular/endothelial dysfunction.

* The most common cause of erectile dysfunction is a vascular disease resulting in endothelial dysfunction

Once you rule out hormonal a Duplex ultrasound would be your best bet as it can rule out vascular causes of ED as it can assess blood flow within the penile arteries/veins, helping to distinguish between arterial insufficiency and venous leak.

*Many patients will respond to initial conservative therapy such as lifestyle maneuvers or oral medications and may not require an additional medical workup; however, patients suffering from moderate to more severe ED often require a more in-depth workup. Severe erectile dysfunction may indicate an improper arterial and venous response to PDE5Is or other vasoactive medications. In such situations, PDDU can clarify the inadequate vascular response.







* a normal erection is mediated by three factors, adequate arteries, adequate venous system and an adequate set of nerves

* ED is typically classified as psychogenic or organic.22 The pathogenesis of ED is multifactorial and can involve multiple underlying disturbances, including vasculogenic, neurogenic, hormonal, and/or medication-induced.

* Although most men with ED do not have hypogonadism, ED has been shown to be related to low T levels in some cases. It has been postulated that T may exert local effects to mediate erections based on studies demonstrating fluctuations in serum and corporal T levels during erection.23 Studies have shown that once T drops below a threshold of roughly 230 ng/dL, men can begin to experience ED.21 This is particularly relevant for men undergoing ADT, for whom ED is a well-established potential side effect. Further research is being undertaken to better understand the mechanisms by which hypogonadism affects erectile function.

* Low testosterone levels can decrease sex drive and lead to weak erections, though this is rarely the sole cause of erectile dysfunction.

High-frequency ultrasound for penile evaluation in ED diagnosis

Abstract High-frequency ultrasound is the imaging modality of choice for evaluating penile pathology because of its easy access, low cost, and patient tolerance (The Penis, Diagnostic Ultrasound, second edition. Boca Raton: CRC Press; 2007:957–978). This pictorial review will illustrate the...

www.excelmale.com

*Erectile dysfunction is a common condition, defined as the inability to attain or maintain penile erections of sufficient quality to allow satisfactory sexual activity. Approximately half of the men between ages 40 and 70 years experience erectile dysfunction, with physical or organic, psychologic, and pharmacologic etiologies.18 The most common cause of erectile dysfunction is a vascular disease resulting in endothelial dysfunction; comorbidity with cardiovascular disease, diabetes mellitus, hyperlipidemia, and hypertension is frequent.19 Duplex ultrasound can evaluate for vascular causes of erectile dysfunction and distinguish between arterial inflow and venous leakage.

Penile Doppler and Ultrasonography for ED

A Review on Penile Doppler and Ultrasonography for Erectile Dysfunction (2022) Kareem Elgendi · Nicholas Zulia · Jonathan Beilan Abstract Purpose of Review Herein, we seek to review the clinical applications of penile duplex Doppler ultrasound (PDDU) in sexual medicine practices and discuss...

www.excelmale.com

The causes of erectile dysfunction are divided into multiple categories including psychogenic, anatomic, neurogenic, vasculogenic, and drug-induced. To properly diagnose and treat ED, a full medical history and physical exam are necessary. Among the various etiologies of ED, vascular pathology has gained a particular interest within the clinical field due to its high association with cardiovascular events (CVEs) and other comorbid conditions.
------------
The first proposed method to diagnose vascular ED involved penile intracavernosal injection (ICI) with a vasoactive medication such as alprostadil [3]. The injection aims to induce an immediate erection by increasing arterial inflow and reducing venous outflow. In early studies, the length and circumference of the penis were measured after injection to determine if there was a vascular abnormality [3]. The use of ICI was a therapeutic approach for ED before oral PDE-5 inhibitors (PDE5i’s) were introduced. However, since this method alone fails to detect the difference between arterial and venous ED, penile duplex Doppler ultrasound (PDDU) has become a popular adjunct to determine a more accurate diagnosis. This review focuses on the clinical applications of PDDU in diagnosing erectile dysfunction and Peyronie’s disease (PD) and discusses recent studies regarding the advantages and limitations of this diagnostic modality.



Clinical Evaluation/Patient History

Collecting a detailed past medical history is paramount in the initial clinical assessment of erectile dysfunction. Important variables within the past medical history include age, a history of smoking, diabetes, hypertension, obesity, dyslipidemia, coronary artery disease, and CVEs such as heart attack and stroke. Psychosocial history and a history of hypogonadism should also be elucidated [4•]. Further basic medical testing consists of a review of the patient's medication list, a focused physical exam, an analysis of contributing psychosocial factors, and subjective questionnaires. The 2018 AUA guidelines on ED recommend the use of validated questionnaires to assess and qualify the severity of ED, as well as provide a platform from which to discuss future management options (expert opinion) [4•]. Many patients will respond to initial conservative therapy such as lifestyle maneuvers or oral medications and may not require an additional medical workup; however, patients suffering from moderate to more severe ED often require a more in-depth workup. Severe erectile dysfunction may indicate an improper arterial and venous response to PDE5Is or other vasoactive medications. In such situations, PDDU can clarify the inadequate vascular response.



The association between ED and cardiovascular disease is relatively high, which has led to vasculogenic etiologies becoming a focused area of study in an effort to prevent future cardiovascular events and improve patient outcomes [3]. These vascular causes include endothelial dysfunction, arterial insufficiency, venous leak, and mixed arterial and venous insufficiency (indeterminate). In order to isolate vascular from nonvascular causes of ED, PDDU has been proven to be an effective diagnostic tool to measure penile blood flow.

Physiology of Erection and Erectile Dysfunction

Physiology of Erection and Pathophysiology of Erectile Dysfunction (2021) Susan M MacDonald, Arthur L Burnett INTRODUCTION The complex pathway from sexual arousal to penile erection has been elucidated in great detail. Advances in neuroimaging have delineated the cortical and limbic system...

www.excelmale.com

*ED often is the end result of multiple pathophysiologic processes

*Arteriogenic ED, which accounts for a majority of cases, has been strongly linked to the following conditions: hypertension, hyperlipidemia, tobacco use, metabolic syndrome/obesity, sedentary lifestyle, diabetes, and pelvic radiation.33–38 Doppler ultrasound has been used to correlate decreased peak systolic velocity of the cavernosal arteries with underlying vascular disease and risk of cardiovascular events.39,40

*The pathologic mechanism underlying arteriogenic ED is likely multifactorial, including 1 or more of the following, as suggested by Musicki and colleagues41 in a 2015 review: (1) endothelial dysfunction, (2) smooth muscle alterations, (3) autonomic dysregulation (discussed later), (4) hypogonadism (see endocrine section), and (5) metabolic defects

*Alterations of vascular smooth muscle content and function have been suggested as contributing factors to ED

*There is a complex relationship between ED and serum testosterone levels

*Further support for the androgen-dependent extent of erectile function includes a threshold testosterone value of 200 ng/dL for regular nocturnal erections

*Studies have demonstrated that testosterone and DHT stimulate nNOS gene expression and increase NO in the corpora during erections.72,74 Van den Broeck and colleagues75 confirmed dose-dependent relaxation of human corpora cavernosal tissue with increasing testosterone and DHT

*Hyperprolactinemia results in reproductive as well as sexual dysfunction. Symptoms associated with hyperprolactinemia include loss of libido, ED, galactorrhea, gynecomastia, and infertility. These symptoms typically occur only at severely elevated levels (>35 ng/mL or 735 mU/L).76

*Hyperthyroidism or hypothyroidism also may be associated with ED.

*A direct effect of thyroxine may also be at play in thyroid hormone ED because both alpha and beta thyroxine receptors have been shown to be present in endothelial and smooth muscle cells from human corpora cavernosa.82

*Psychogenic ED may not be a primary etiology in most cases but it is a contributing factor in virtually all cases

*The degree to which ED is psychogenic versus physiologic is difficult to parse out; isolated psychogenic ED is considered a diagnosis of exclusion clinically.

Radiologic Approach to Erectile Dysfunction. Main causes, diagnosis and therapeutic options in interventional radiology

Learning objectives Learn about erectile dysfunction. Pathophysiology, symptoms and main causes. Stimulated Color Doppler ultrasound diagnostic criteria. Arteriogenic erectile dysfunction, veno-occlusive erectile dysfunction , mixed aetiology and false venous-leak. Role of interventional...

www.excelmale.com

Look over the threads in post #4!

What to Do About Erectile Dysfunction

https://www.nytimes.com/2024/06/27/well/live/advice-erectile-dysfunction-treatment.html Sooner or later, most men will experience a problem achieving or maintaining an erection. But today, there are more treatments than ever. Erectile dysfunction is more common than one might think. More...

www.excelmale.com

Efficient use of penile Doppler ultrasound for investigating men with ED

https://academic.oup.com/jsm/article-abstract/21/8/734/7725387?redirectedFrom=fulltext Introduction Current evidence demonstrates that >80% of patients with erectile dysfunction (ED) have some underlying organic etiology.1 Among organic causes, vasculogenic ED is the most common.1...

www.excelmale.com

Take-home message

PDUS is a valuable minimally invasive tool for erectile hemodynamic assessment in men with ED and can aid in delineating the etiology of ED and thus guide its management. PDUS should be conducted only by clinicians who have received formal training in the performance of PDUS and analysis of the data generated. There is a dire need for standardization of PDUS protocols. Redosing of a vasoactive agent and the availability of audiovisual sexual stimulation are useful to maximize complete cavernosal SMR, which is critical for the generation of reliable data. For this reason, we suggest the utilization of a rigidity-based assessment during PDUS. PDUS should be performed after the patient achieves full erection hardness or the maximum dose of the vasoactive agent has been administered. We recommend a PSV cutoff of <30 cm/s to diagnose arterial insufficiency and an EDV cutoff of ≥5 cm/s to diagnose CVOD. Finally, all patients must achieve detumescence below penetration hardness before discharge.


*Current evidence demonstrates that >80% of patients with erectile dysfunction (ED) have some underlying organic etiology.1

*Among organic causes, vasculogenic ED is the most common.1 Vasculogenic ED includes insufficient arterial inflow (arterial insufficiency), corporal veno-occlusive dysfunction (CVOD), or mixed vasculogenic ED (arterial insufficiency + CVOD).2

*Expert opinion statements state that specialized testing may be required for individuals with more complex histories and presentations of ED. Among others, such advanced tests include penile Doppler ultrasound (PDUS).3-7 The European Association of Urology guidelines for sexual and reproductive health describe PDUS as a second level diagnostic test to evaluate the hemodynamics of erectile function, and it is usually used in conditions associated with a vasculogenic etiology of ED.7

*PDUS assesses corpus cavernosal structure and function (hemodynamics)3 and has emerged as the gold standard for penile vascular assessment.4

*PDUS represents the gold standard test for erectile hemodynamics assessment despite not being 100% accurate.

*PDUS proves invaluable in distinguishing non vasculogenic (normal hemodynamics, most often psychogenic ED) and vasculogenic etiologies.The accuracy of PDUS is predicated on the achievement of complete cavernosal smooth muscle relaxation (SMR), most often signified by high-end erection rigidity or the presence of negative end diastolic velocities (EDVs; Figure 2).12,13

Preventing and treating erectile dysfunction with Dr. Mohit Khera

* the best ways to think about the causes for erectile dysfunction is to use the mnemonic VENT (vascular, endocrine, neurologic, trauma) * VASCULAR being the MOST COMMON cause! Dr. Mohit Khera, professor of Urology at Baylor College of Medicine talks about men's health topics such as...

www.excelmale.com

* the best ways to think about the causes for erectile dysfunction is to use the mnemonic VENT (vascular, endocrine, neurologic, trauma)

* VASCULAR being the MOST COMMON cause!



post #23

The Value of Penile Ultrasound in ED Diagnosis

www.excelmale.com

Erectile Dysfunction Treatment: State of the Art Care in 2024

www.excelmale.com

*57% of all men with ED have moderate/severe ED

Androgens and ED: from androgen deficiency to treatment

Abstract Introduction Androgens play important roles in regulating the growth and development of the male reproductive system and maintaining libidoand erectile function. The specific mechanisms by which androgen deficiency leads to erectile dysfunction (ED) are not yet fully understood...

www.excelmale.com

*The process of male penile erection is complex in that it requires blood vessels, nerves, and muscles to work together; thus, the structural and functional integrity of these tissues plays an important role in penile erection

*Androgen deficiency can lead to ED by inhibiting the NOS/NO/cGMP pathway (nitric oxide synthase/nitric oxide/cyclic guanosine monophosphate) and altering the expression of ion channel proteins, as well as by inducing oxidative stress, death, and fibrosis in penile corpus cavernosum cells

*The NO/cyclic guanosine monophosphate(NO/cGMP) signaling pathway may be the most important pathway that acts on the penile vasculature and smooth muscle; it also plays an important regulatory role in the erectile process

*Nerve cells and endothelial cells in the corpus cavernosum produce and release NO synthase (NOS), which activates guanylyl cyclase and produces cGMP; this reduces the inward flow of Ca+, leading to smooth muscle relaxation and penile erection



post#2

Sildenafil, 25 Years Later

Sildenafil: 25 Years Later – Summary Twenty-five years ago, the FDA’s approval of sildenafil (Viagra) radically reshaped the treatment of erectile dysfunction. Editor-in-Chief of Grand Rounds in Urology, E. David Crawford, MD, sits down to discuss the history and future of PDE5 inhibitors with...

www.excelmale.com

 

[madman]

Well I gained all this knowledge, because I had no choice, but to go deeper. Unfortunately I have fixed my hormones now to a high degree and have massive symptom relief, other than libido, so it works quite well. Overall there is no pride or ego in this knowledge, I'd much rather have great success immediately upon starting TRT and forget about all this, but what can you do. In the end you can feel limited results and either accept this state or start experimenting more to find a solution. Experiment or don't, you won't feel amazing either way until you find something, so might as well do something that will hopefully deal with your issues in the future. Doing it systematically and getting regularly tested just ensures that you have the best possible approach and data. Considering you mentioned that you have a great symptom relief for weeks and then you suddenly crash, I think it's safe to assume that it's hormonal. In my case my libido has been at a constant 0, regardless of what I've tried, so I think the problem is something additional to hormones.


Well it also depends on how long you've been doing TRT before adding HCG. So how much atrophy you have before HCG. I was on TRT for 2 years with Test E before adding HCG and 500 IU/week wasn't enough to do anything, because I was already suppressed for so long. In this case people take much higher doses to kick start their system and then reduce the dose to maintain. I did 3000 IU/week split into 3 doses for 1.5 months to get my testicles back to 100%, then I did 600 IU/week split into 2 doses to maintain. Soon after switching to Test P I also dropped HCG due to traveling and I only have minor atrophy compared to a longer ester. I'd say on Test P I only lost about 15-20% of the size, and I have no aching (huge plus), meanwhile on Test E I lost 50-60%. Constant levels of hormones and higher doses suppress a lot more.

Constant levels of hormones and higher doses suppress a lot more.


Much more to the story here!

Formulation/PKs, dosing protocol/minimum effective doses needed to raise T levels in order to achieve a healthy FT level in order to provide relief/improvement of symptoms will results in suppression of the hpta.

Nateso T gel is the only formulation that will cause the least suppression of the hpta due to the PK/dosing protocol.

Natesto is meant to/needs to be applied intranasally in order to reap the benefits of the PK.

In and out of your system quickly due to the half-life of unesterified T.

Dosed 2-3 times daily which results in a short-lived peak with long trough times between doses.

*The key point here is a short-lived peak with long trough times between doses.

As I stated in a previous thread when using daily short-acting TP the T levels achieved peak vs trough let alone the time period over those 24 hrs T levels are elevated whether mid-range/high/absurdly high will still result in a strong suppression of the hpta.

Top it off there are many injecting daily TP hitting very high/absurdly high peaks let alone healthy troughs.

T Propionate protocol

Well only 8mg of straight Prop peaked me at 1200 TT ! since Tprop would quickly taper off question is how long after injection. TBH the blood levels are way overvalued by most in T community. most of the action happens at the receptor you can't measure that. i completely ignore all those...

www.excelmale.com

Natural Test Shut Down

Howdy, Basic question--I tried the search feature but could not find definitive information on the following. The specific question: Is there a dosing of Testosterone Enanthate (in mg per week) below which you can expect to preserve what is left of natural testosterone production? Does the...

www.excelmale.com

My clinic says gel is less suppressive than injectables and easier to come off

I’ve been on TRT for coming up to 3 years. Due to having various issues with it, I am considering trying to come off it. I was on cypionate for 1.5 years, then sustanon for a year and now testogel for last 4/5 months. I enquired about stopping with my clinic and they said that gel was less...

www.excelmale.com

Soon after switching to Test P I also dropped HCG due to traveling and I only have minor atrophy compared to a longer ester. I'd say on Test P I only lost about 15-20% of the size, and I have no aching (huge plus), meanwhile on Test E I lost 50-60%.


Again the only way for an individual to truly know would be to have testicular volume measured using a prader orchidometer or ultrasonography pre/post TRT.

You would never truly know playing the guessing game!

 

[madman]

OP had a problem with his TRT protocol, he had results, but were inconsistent due to the "crashes" he experienced. I provided some information and a plan to hopefully help him dial in. I didn't see a need to go in dept about lifestyle or thyroid hormones or anything similar as I think someone on TRT should already realize these things, especially if he was dealing with decent doctors, so I considered it off topic. Of course if he hasn't checked these things or got them in order, then it would make sense to do so.


OP was already using higher doses than what I recommended, and he has the blood tests done, so I think it was a good dose and protocol adjustment recommendation. I know that full blood panels are better, and I personally have quite many, but after a few you already see a pattern. Someone with low SHBG is not going to magically have high SHBG suddenly, so you can make an accurate prediction on where things stand. In my post I just inserted a snippet of my blood panel, as the rest wasn't relevant, it was fine. For my experimentation my point was to get a feel where I stand and how I feel, and it was not economical or made sense, in my opinion, to do a comprehensive blood panel every time. I realize what I was doing, I wanted to try a higher doses for a while to see if anything would improve/change, but it didn't so I started lowering it soon after, and started trying lower doses.

In any case this is a bit off topic as it's more about what I was doing back then, than what OP is facing and doing now.

You clearly had no clue where the most important blood marker FT sat!

That daily dose 17.5 mg TP (122.5 mg/week) that you recommended to the OP is not a low starting dose!

Again as you should very well know TP has more active T/mg.

We can nitpick here on the approx free equivalents but you get the point!

122.5 mg TP (101.6 mg active T)/week would be the equivalent of banging roughly 145 mg TC (101.5 mg active T)/week.

Common starting dose when using TC/TE would be 100 mg/week (70-72 mg active T)!

If we are talking about starting someone on low dose daily TP then 10-12 mg (70-84 mg TP/week) would be where it's at!

 

[Spartan1985]

When it comes to the hormonal aspect having healthy FT, DHT and estradiol levels are critical!

Low levels of any of these hormones would have a negative impact on libido/erectile function.

One does not need high FT let alone DHT in order to have a healthy libido/erectile function.

It's myth that high T will have one running around with a raging libido and titanium erections to boot!

When it comes to using exogenous T having too high a FT especially steady-state can be just as bad in many ways as having too low a FT level especially when it comes to libido and erectile function.

Skewed T:E ration can have a negative impact.

Dysfunction thyroid/adrenals can have a negative impact on libido/erectile function.

Elevated prolactin can have a negative impact on libido/erections.

* Hyperprolactinemia results in reproductive as well as sexual dysfunction. Symptoms associated with hyperprolactinemia include loss of libido, ED, galactorrhea, gynecomastia, and infertility. These symptoms typically occur only at severely elevated levels (>35 ng/mL or 735 mU/L).76

High blood pressure, hyperlipidemia and high blood sugar can damage blood vessels/nerves.

Adrenaline is a libido/EF killer!

* Adrenalin.....anti-erection chemical!

As I stated in a previous thread.

Libido starts in the brain.

Neurotransmitters have a big impact especially dopamine.

There is a fine balance here when it comes to the dopamine system!

This is key here..... dopamine circuits are powerfully regulated by androgens!

Hammering the shit out of your dopamine is the last thing you want to do.

Anything that lowers libido can lead to ED if the drive is absent!

Even then for the majority of older men ED is vasculogenic!

By the time one hits 40 many men will experience some degree of ED (mild, moderate, severe) due to vascular/endothelial dysfunction.

* The most common cause of erectile dysfunction is a vascular disease resulting in endothelial dysfunction

Once you rule out hormonal a Duplex ultrasound would be your best bet as it can rule out vascular causes of ED as it can assess blood flow within the penile arteries/veins, helping to distinguish between arterial insufficiency and venous leak.

*Many patients will respond to initial conservative therapy such as lifestyle maneuvers or oral medications and may not require an additional medical workup; however, patients suffering from moderate to more severe ED often require a more in-depth workup. Severe erectile dysfunction may indicate an improper arterial and venous response to PDE5Is or other vasoactive medications. In such situations, PDDU can clarify the inadequate vascular response.







* a normal erection is mediated by three factors, adequate arteries, adequate venous system and an adequate set of nerves

* ED is typically classified as psychogenic or organic.22 The pathogenesis of ED is multifactorial and can involve multiple underlying disturbances, including vasculogenic, neurogenic, hormonal, and/or medication-induced.

* Although most men with ED do not have hypogonadism, ED has been shown to be related to low T levels in some cases. It has been postulated that T may exert local effects to mediate erections based on studies demonstrating fluctuations in serum and corporal T levels during erection.23 Studies have shown that once T drops below a threshold of roughly 230 ng/dL, men can begin to experience ED.21 This is particularly relevant for men undergoing ADT, for whom ED is a well-established potential side effect. Further research is being undertaken to better understand the mechanisms by which hypogonadism affects erectile function.

* Low testosterone levels can decrease sex drive and lead to weak erections, though this is rarely the sole cause of erectile dysfunction.

High-frequency ultrasound for penile evaluation in ED diagnosis

Abstract High-frequency ultrasound is the imaging modality of choice for evaluating penile pathology because of its easy access, low cost, and patient tolerance (The Penis, Diagnostic Ultrasound, second edition. Boca Raton: CRC Press; 2007:957–978). This pictorial review will illustrate the...

www.excelmale.com

*Erectile dysfunction is a common condition, defined as the inability to attain or maintain penile erections of sufficient quality to allow satisfactory sexual activity. Approximately half of the men between ages 40 and 70 years experience erectile dysfunction, with physical or organic, psychologic, and pharmacologic etiologies.18 The most common cause of erectile dysfunction is a vascular disease resulting in endothelial dysfunction; comorbidity with cardiovascular disease, diabetes mellitus, hyperlipidemia, and hypertension is frequent.19 Duplex ultrasound can evaluate for vascular causes of erectile dysfunction and distinguish between arterial inflow and venous leakage.

Penile Doppler and Ultrasonography for ED

A Review on Penile Doppler and Ultrasonography for Erectile Dysfunction (2022) Kareem Elgendi · Nicholas Zulia · Jonathan Beilan Abstract Purpose of Review Herein, we seek to review the clinical applications of penile duplex Doppler ultrasound (PDDU) in sexual medicine practices and discuss...

www.excelmale.com

The causes of erectile dysfunction are divided into multiple categories including psychogenic, anatomic, neurogenic, vasculogenic, and drug-induced. To properly diagnose and treat ED, a full medical history and physical exam are necessary. Among the various etiologies of ED, vascular pathology has gained a particular interest within the clinical field due to its high association with cardiovascular events (CVEs) and other comorbid conditions.
------------
The first proposed method to diagnose vascular ED involved penile intracavernosal injection (ICI) with a vasoactive medication such as alprostadil [3]. The injection aims to induce an immediate erection by increasing arterial inflow and reducing venous outflow. In early studies, the length and circumference of the penis were measured after injection to determine if there was a vascular abnormality [3]. The use of ICI was a therapeutic approach for ED before oral PDE-5 inhibitors (PDE5i’s) were introduced. However, since this method alone fails to detect the difference between arterial and venous ED, penile duplex Doppler ultrasound (PDDU) has become a popular adjunct to determine a more accurate diagnosis. This review focuses on the clinical applications of PDDU in diagnosing erectile dysfunction and Peyronie’s disease (PD) and discusses recent studies regarding the advantages and limitations of this diagnostic modality.



Clinical Evaluation/Patient History

Collecting a detailed past medical history is paramount in the initial clinical assessment of erectile dysfunction. Important variables within the past medical history include age, a history of smoking, diabetes, hypertension, obesity, dyslipidemia, coronary artery disease, and CVEs such as heart attack and stroke. Psychosocial history and a history of hypogonadism should also be elucidated [4•]. Further basic medical testing consists of a review of the patient's medication list, a focused physical exam, an analysis of contributing psychosocial factors, and subjective questionnaires. The 2018 AUA guidelines on ED recommend the use of validated questionnaires to assess and qualify the severity of ED, as well as provide a platform from which to discuss future management options (expert opinion) [4•]. Many patients will respond to initial conservative therapy such as lifestyle maneuvers or oral medications and may not require an additional medical workup; however, patients suffering from moderate to more severe ED often require a more in-depth workup. Severe erectile dysfunction may indicate an improper arterial and venous response to PDE5Is or other vasoactive medications. In such situations, PDDU can clarify the inadequate vascular response.



The association between ED and cardiovascular disease is relatively high, which has led to vasculogenic etiologies becoming a focused area of study in an effort to prevent future cardiovascular events and improve patient outcomes [3]. These vascular causes include endothelial dysfunction, arterial insufficiency, venous leak, and mixed arterial and venous insufficiency (indeterminate). In order to isolate vascular from nonvascular causes of ED, PDDU has been proven to be an effective diagnostic tool to measure penile blood flow.

Physiology of Erection and Erectile Dysfunction

Physiology of Erection and Pathophysiology of Erectile Dysfunction (2021) Susan M MacDonald, Arthur L Burnett INTRODUCTION The complex pathway from sexual arousal to penile erection has been elucidated in great detail. Advances in neuroimaging have delineated the cortical and limbic system...

www.excelmale.com

*ED often is the end result of multiple pathophysiologic processes

*Arteriogenic ED, which accounts for a majority of cases, has been strongly linked to the following conditions: hypertension, hyperlipidemia, tobacco use, metabolic syndrome/obesity, sedentary lifestyle, diabetes, and pelvic radiation.33–38 Doppler ultrasound has been used to correlate decreased peak systolic velocity of the cavernosal arteries with underlying vascular disease and risk of cardiovascular events.39,40

*The pathologic mechanism underlying arteriogenic ED is likely multifactorial, including 1 or more of the following, as suggested by Musicki and colleagues41 in a 2015 review: (1) endothelial dysfunction, (2) smooth muscle alterations, (3) autonomic dysregulation (discussed later), (4) hypogonadism (see endocrine section), and (5) metabolic defects

*Alterations of vascular smooth muscle content and function have been suggested as contributing factors to ED

*There is a complex relationship between ED and serum testosterone levels

*Further support for the androgen-dependent extent of erectile function includes a threshold testosterone value of 200 ng/dL for regular nocturnal erections

*Studies have demonstrated that testosterone and DHT stimulate nNOS gene expression and increase NO in the corpora during erections.72,74 Van den Broeck and colleagues75 confirmed dose-dependent relaxation of human corpora cavernosal tissue with increasing testosterone and DHT

*Hyperprolactinemia results in reproductive as well as sexual dysfunction. Symptoms associated with hyperprolactinemia include loss of libido, ED, galactorrhea, gynecomastia, and infertility. These symptoms typically occur only at severely elevated levels (>35 ng/mL or 735 mU/L).76

*Hyperthyroidism or hypothyroidism also may be associated with ED.

*A direct effect of thyroxine may also be at play in thyroid hormone ED because both alpha and beta thyroxine receptors have been shown to be present in endothelial and smooth muscle cells from human corpora cavernosa.82

*Psychogenic ED may not be a primary etiology in most cases but it is a contributing factor in virtually all cases

*The degree to which ED is psychogenic versus physiologic is difficult to parse out; isolated psychogenic ED is considered a diagnosis of exclusion clinically.

Radiologic Approach to Erectile Dysfunction. Main causes, diagnosis and therapeutic options in interventional radiology

Learning objectives Learn about erectile dysfunction. Pathophysiology, symptoms and main causes. Stimulated Color Doppler ultrasound diagnostic criteria. Arteriogenic erectile dysfunction, veno-occlusive erectile dysfunction , mixed aetiology and false venous-leak. Role of interventional...

www.excelmale.com

Look over the threads in post #4!

What to Do About Erectile Dysfunction

https://www.nytimes.com/2024/06/27/well/live/advice-erectile-dysfunction-treatment.html Sooner or later, most men will experience a problem achieving or maintaining an erection. But today, there are more treatments than ever. Erectile dysfunction is more common than one might think. More...

www.excelmale.com

Efficient use of penile Doppler ultrasound for investigating men with ED

https://academic.oup.com/jsm/article-abstract/21/8/734/7725387?redirectedFrom=fulltext Introduction Current evidence demonstrates that >80% of patients with erectile dysfunction (ED) have some underlying organic etiology.1 Among organic causes, vasculogenic ED is the most common.1...

www.excelmale.com

Take-home message

PDUS is a valuable minimally invasive tool for erectile hemodynamic assessment in men with ED and can aid in delineating the etiology of ED and thus guide its management. PDUS should be conducted only by clinicians who have received formal training in the performance of PDUS and analysis of the data generated. There is a dire need for standardization of PDUS protocols. Redosing of a vasoactive agent and the availability of audiovisual sexual stimulation are useful to maximize complete cavernosal SMR, which is critical for the generation of reliable data. For this reason, we suggest the utilization of a rigidity-based assessment during PDUS. PDUS should be performed after the patient achieves full erection hardness or the maximum dose of the vasoactive agent has been administered. We recommend a PSV cutoff of <30 cm/s to diagnose arterial insufficiency and an EDV cutoff of ≥5 cm/s to diagnose CVOD. Finally, all patients must achieve detumescence below penetration hardness before discharge.


*Current evidence demonstrates that >80% of patients with erectile dysfunction (ED) have some underlying organic etiology.1

*Among organic causes, vasculogenic ED is the most common.1 Vasculogenic ED includes insufficient arterial inflow (arterial insufficiency), corporal veno-occlusive dysfunction (CVOD), or mixed vasculogenic ED (arterial insufficiency + CVOD).2

*Expert opinion statements state that specialized testing may be required for individuals with more complex histories and presentations of ED. Among others, such advanced tests include penile Doppler ultrasound (PDUS).3-7 The European Association of Urology guidelines for sexual and reproductive health describe PDUS as a second level diagnostic test to evaluate the hemodynamics of erectile function, and it is usually used in conditions associated with a vasculogenic etiology of ED.7

*PDUS assesses corpus cavernosal structure and function (hemodynamics)3 and has emerged as the gold standard for penile vascular assessment.4

*PDUS represents the gold standard test for erectile hemodynamics assessment despite not being 100% accurate.

*PDUS proves invaluable in distinguishing non vasculogenic (normal hemodynamics, most often psychogenic ED) and vasculogenic etiologies.The accuracy of PDUS is predicated on the achievement of complete cavernosal smooth muscle relaxation (SMR), most often signified by high-end erection rigidity or the presence of negative end diastolic velocities (EDVs; Figure 2).12,13

Preventing and treating erectile dysfunction with Dr. Mohit Khera

* the best ways to think about the causes for erectile dysfunction is to use the mnemonic VENT (vascular, endocrine, neurologic, trauma) * VASCULAR being the MOST COMMON cause! Dr. Mohit Khera, professor of Urology at Baylor College of Medicine talks about men's health topics such as...

www.excelmale.com

* the best ways to think about the causes for erectile dysfunction is to use the mnemonic VENT (vascular, endocrine, neurologic, trauma)

* VASCULAR being the MOST COMMON cause!



post #23

The Value of Penile Ultrasound in ED Diagnosis

www.excelmale.com

Erectile Dysfunction Treatment: State of the Art Care in 2024

www.excelmale.com

*57% of all men with ED have moderate/severe ED

Androgens and ED: from androgen deficiency to treatment

Abstract Introduction Androgens play important roles in regulating the growth and development of the male reproductive system and maintaining libidoand erectile function. The specific mechanisms by which androgen deficiency leads to erectile dysfunction (ED) are not yet fully understood...

www.excelmale.com

*The process of male penile erection is complex in that it requires blood vessels, nerves, and muscles to work together; thus, the structural and functional integrity of these tissues plays an important role in penile erection

*Androgen deficiency can lead to ED by inhibiting the NOS/NO/cGMP pathway (nitric oxide synthase/nitric oxide/cyclic guanosine monophosphate) and altering the expression of ion channel proteins, as well as by inducing oxidative stress, death, and fibrosis in penile corpus cavernosum cells

*The NO/cyclic guanosine monophosphate(NO/cGMP) signaling pathway may be the most important pathway that acts on the penile vasculature and smooth muscle; it also plays an important regulatory role in the erectile process

*Nerve cells and endothelial cells in the corpus cavernosum produce and release NO synthase (NOS), which activates guanylyl cyclase and produces cGMP; this reduces the inward flow of Ca+, leading to smooth muscle relaxation and penile erection



post#2

Sildenafil, 25 Years Later

Sildenafil: 25 Years Later – Summary Twenty-five years ago, the FDA’s approval of sildenafil (Viagra) radically reshaped the treatment of erectile dysfunction. Editor-in-Chief of Grand Rounds in Urology, E. David Crawford, MD, sits down to discuss the history and future of PDE5 inhibitors with...

www.excelmale.com

Thanks for taking the time to provide such a detailed answer you clearly know truly how these things work. Wish my urologist had that level of knowledge to be honest. I’ve been referred to a regional urologist and will request the ultrasound you mentioned I have looked for a private company that do it but can’t find anyone in Scotland who offers that.

I’m working on developing my cardiovascular fitness which took a major hit after the health scare a few years back that started this whole process as I do agree that is a major component of trying to get proper functionality. I will take your advice on the 10-12mg when I start daily dosing at the end of this week also, I definitely think I’ve felt the affects of the dopamine impact with higher doses so far.

A lot of the science within your answer is a little outwith my understanding at this stage but my major take is that you have confirmed that the answer may not truly be in the hormones although after clear issues with high E2 impacting erection quality so far and crashes with AI I definitely need to get the protocol as accurate as possible to get a better idea of how severe the issue is once the exogenous inputs are at the correct level.

Thanks again for spending the time putting this together in response it’s very much appreciated. Pity you are not local and running a male health service as with the knowledge you have im fairly sure the cause of this would be found.

Take care

 

[madman]

Dr John Mulhall, MD - 70% of ED cases are vascular!

One of the top in the field love this guy! Mulhall always breaks it down! Listen closely as he hits the nail on the HEAD! 3:33-7:13 * if you look at men with ORGANIC ED we can talk about psychogenic ED a little later on if we have time but if you take men with ORGANIC ED PROBABLY 70% OF...

www.excelmale.com

3:33-7:13

* if you look at men with ORGANIC ED we can talk about psychogenic ED a little later on if we have time but if you take men with ORGANIC ED PROBABLY 70% OF THEM ARE GOING TO HAVE A VASCULAR COMPONENT INFLOW OR OUTFLOW PROBLEMS and that includes men with diabetes, those high profile causes like medication induced or hormonal ED or Arteriogenic ED, radical pelvic surgery for example account for the vast minority of patients with erectile dysfunction and if you focus in on HORMONE PROBLEMS such as TESTOSTERONE that accounts for the VAST MINORITY of MEN with ERECTION PROBLEMS so the BULK of ED that's PHYSICALLY BASED is VASCULOGENIC as its called!


* the whole link between TESTOSTERONE and ERECTILE FUNCTION it's a WEAK LINK, it's not a POTENT ERECTO-GENIC HORMONE, it's CERTAINLY a LIBDO-GENIC HORMONE and an ORGASMO-GENIC HORMONE but if you take men who have got LOW TESTOSTERONE who have ERECTILE DYSFUNCTION and you treat them with T the AVERAGE CHANGE in ERECTILE FUNCTION is MINIMAL if you use the validated scores (the international index of erectile function scores) so the ELEVATION in those scores is MINIMAL so the CONTRIBUTION of T you DON'T NEED A LOT of T you need SOME you DON'T NEED A LOT of T for ERECTION FUNCTION!




What role does DHT (dihydrotestosterone) play with erections?


9:33-11:54

* it is CERTAINLY ALL ANDROGENS are involved in ERECTILE TISSUE HEALTH and ERECTILE FUNCTION but as an ANDROGEN PERTAINING SPECIFICALLY to ERECTILE HEALTH it is NOT the MAJOR PLAYER TESTOSTERONE ITSELF would be MORE IMPORTANT!

 

[ed031561]

Long story but thought overview would be best. Major health issue 2020 with oesophageal bleed which was put down to long term steroid use. Nearly died, double blood transfusion and was told to not take any PCT as my body would recover in time (was 35 at the time) over a year later and no recovery so TRT company started me on TRT. Absolute nightmare ever since, various dosage alterations, different TRT companies and ED plus low libido etc still as bad as before it started. Been on low dose, high dose, various esters and nothing seems to work for more than a few weeks then crashes again. Pretty sure it’s something to do with oestrogen levels and AI use not sitting well with my body, seems even low dose fortnightly can crash things. Last blood tests (attached) came back and TRT doc said I should feel great on those numbers. No sex drive, brain fog and ED issues still major problem. Can’t remember my last morning erection and need high dose viagra 200mg to do anything and even that’s only 7/10 at best. Thought I’d reach out and see if anyone at all has any ideas or input at this stage? Tempted to just taper off and accept defeat but at 39 and the mrs blaming herself that’s going to be a disaster also.

Anyone not responded to TRT at all or had major issues finding any balance? Or anyone else really struggled with oestrogen management?

NHS endocrinologist has said to stop listening to TRT company as they promote bad protocol and said 250mg of sustanon once every 3 weeks is all they would suggest. Urology have said nothing physically wrong so must be hormonal.

Really wish I hadn’t started and feel completely lost at this stage

If your taking any type of AI or aromatase blocker, stop!

 

[madman]

Sexual Dysfunction - A General Approach

1:25:20-2:14:20 Take home points: * ERECTILE DYSFUNCTION (ORGANIC/PSYCHOGENIC) * 90% of the patient will have an ORGANIC CAUSE * ORGANIC is usually very PROGRESSIVE * at 70 YRS old 2/3 of men will have SOME DEGREE of ERECTILE DYSFUNCTION * 2 types of erection...

www.excelmale.com

Take home points:


* ERECTILE DYSFUNCTION (ORGANIC/PSYCHOGENIC)

* 90% of the patient will have an ORGANIC CAUSE

* ORGANIC is usually very PROGRESSIVE

* at 70 YRS old 2/3 of men will have SOME DEGREE of ERECTILE DYSFUNCTION

* 2 types of erection (psychogenic/reflexogenic)

* in the cell the most important PATHWAY is the NITRIC OXIDE PATHWAY

* the most important NITRIC OXIDE would be from the NERVE ENDING to INDUCE the ERECTION but to MAINTAIN it, it would be the NITRIC OXIDE from the ENDOTHELIUM that would be the MOST IMPORTANT

* the TESTOSTERONE EFFECT is MAINLY on the LIBIDO/SEXUAL DESIRE

* MEDICATIONS the worst are the ANTIHYPERTENSIVES and the 2 worst are the THIAZIDE DIURETIC and the NON-SELECTIVE BETA-BLOCKERS (the old beta blockers)

* when you look OVERALL at THE RISK FACTOR I mean the WORST are the ANTIDEPRESSANTS, second is HYPERTENSION or VASCULAR

* we know now it's almost a PREDICTOR of CARDIOVASCULAR DISEASE

* the LINK between ERECTILE DYSFUNCTION and CARDIOVASCULAR DISEASE is the ENDOTHELIUM or ENDOTHELIUM DYSFUNCTION

* you have to see the ENDOTHELIUM as a LIVE STRUCTURE, I told you the IMPORTANCE of the ENDOTHELIUM is to MAINTAIN the ERECTION by LIBERATION of NITRIC OXIDE during SEXUAL ACTIVITY so it is VERY VERY IMPORTANT

* ONSET OF DYSFUNCTION - GRADUAL is usually ORGANIC except an ACUTE SURGERY whereas PSYCHOGENIC ERECTILE DYSFUNCTION is OFTEN MORE ACUTE

* the WORST TYPE of LIPID is actually the TRIGLYCERIDE if their HIGH they INCREASE the ENDOTHELIAL DYSFUNCTION

* PDE5 DESTROY THE CYCLIC GMP so the PDE5 INHIBITOR that goes with the name they INHIBIT this and then you have a MAXIMUM EFFECT of the CYCLIC GMP and the CALCIUM goes out of the CELL the MUSCLE CELL and you get the MAXIMUM EFFECT ALL THE TIME

Molecular Biology and Physiology of Erectile Function and Dysfunction

36.1 Introduction Erectile dysfunction (ED) refers to the inability to achieve or maintain an erection for satisfactory sexual performance. It is highly prevalent among aging men and can have a significant impact on quality of life and interpersonal relationships [1]. It was estimated in 2000...

www.excelmale.com

Erectile dysfunction - What Is Penile Venous Leakage?

* a normal erection is mediated by three factors, adequate arteries, adequate venous system and an adequate set of nerves Venous leak - the inability to trap blood in the penis 2 clinical tip offs to the presence of venous leak - I've had years of normal erectile function and now no matter...

www.excelmale.com

Venous Leakage in the Penis: Young, Attractive, ... IMPOTENT?

5:25-6:43 (5α-Reductase, scar tissue/venous leak) *dihydrotestosterone is extremely important for the health of the smooth muscle cell of the penis , like really important Here is a nightmare condition in young men: erectile dysfunction due to venous leakage. While it is a neglected...

www.excelmale.com

*Venous leakage occurs when veins in the penis fail to close, preventing blood from being trapped and resulting in erectile dysfunction. Typically, arteries bring oxygenated blood to the penis, while veins return used blood to the heart. In a healthy erection, the veins close, trapping blood in the penis. However, in veno-occlusive erectile dysfunction, the veins stay open, leading to erectile issues

*Factors contributing to venous leakage include abnormal anatomical distribution of veins, excessive fibrosis of erectile tissue, and side effects from medications like SSRIs and Finasteride. These drugs can cause scarring in the penile tissue, leading to venous leakage. But also bike injuries contribute to this complex condition. Likewise, they can cause scarring of the crus of the penis

*Traditional color Doppler ultrasound may miss it, whereas grayscale ultrasound, which requires high-resolution equipment, is more effective

 

[madman]

Dr. Mohit Khera Explains How to CURE Erectile Dysfunction

Pay close attention BRUHS! 7:46-8:44 More T is better forl ibido/erectile function.....NO there is a PLATEAU EFFECT! 4 PILLARS OF HEALTH DESS (Diet; Exercise; Sleep; Stress)

www.excelmale.com

 

[Spartan1985]

If your taking any type of AI or aromatase blocker, stop!

Yeah defo don’t tolerate these well at all they always lead to a crash and going by what other members have been saying the dosages I’ve been prescribed to date are too high so resulting in E2 rising too high causing issues the AI crashing me. Started 10mg test p daily SubQ this week to approach from a different angle, no hcg or AI and see how things settle after a few weeks. Thanks for taking the time to reply to my post much appreciated

 

[madman]

Yeah defo don’t tolerate these well at all they always lead to a crash and going by what other members have been saying the dosages I’ve been prescribed to date are too high so resulting in E2 rising too high causing issues the AI crashing me. Started 10mg test p daily SubQ this week to approach from a different angle, no hcg or AI and see how things settle after a few weeks. Thanks for taking the time to reply to my post much appreciated

$$$

 

[nippy]

All sounds like me .. I've been off trt now for 8 months. NHS did bloods last week . She rang to say my fsh and lh are back to normal and my testosterone too. They didn't measure my free t and my E2 not important they say. So I've requested a copy and I'll work it out myself. I said so why have I still got no erections and libido and loss of penis sensitivity... She replied I don't know your bloods are fine.. sounds like the last trt private doc I was at. Mens health clinic in the UK. I have no idea what to do now. I'm desperate and so depressed