I ordered and have selegiline. However, I am hesitant to take it since its really for parkinsons. So I tried wellbutrin first
sensitivity issue can't solve
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Im 44. I do have selegiline on hand. But I was hesitant to take it since its for parkinsons
So i wanted to try Wellbutrin first and definitely won't be taking both at the same time. What's your dosage on selegiline and frequency. How long have you been on it?
My approach is overly complex and impractical for most; it involves multiple daily injections. It's much simpler to first try significant dose reductions, and if no luck there then try switching to a short-acting form of testosterone, as these resolve hypogonadism with less hormonal chaos than conventional TRT. Your current TRT dose is likely still on the order of double what your healthy natural production would be, which is around 5-7 mg of testosterone daily. This corresponds to 50-70 mg of testosterone cypionate weekly. Excessive testosterone can have negative effects on 20-30+ other hormones and neurotransmitters. My discussion of two of the most directly affected hormones:
In any case, if you can switch to short-acting TRT then your hormones operate closer to normal, reducing the risk of side effects. Short-acting testosterone includes nasal gels, buccal troches and possibly certain oral formulations. The former two are the best proven, but are less convenient. A trial could at least establish whether the approach is helpful to you. These forms of TRT are simpler than trying to directly replace the suppressed GnRH with gonadorelin and the suppressed kisppeptin with kisspeptin-10.
Read some other accounts of the misery caused by excessive TRT dosing:
Especially this one:
I appreciate that.My approach is overly complex and impractical for most; it involves multiple daily injections. It's much simpler to first try significant dose reductions, and if no luck there then try switching to a short-acting form of testosterone, as these resolve hypogonadism with less hormonal chaos than conventional TRT. Your current TRT dose is likely still on the order of double what your healthy natural production would be, which is around 5-7 mg of testosterone daily. This corresponds to 50-70 mg of testosterone cypionate weekly. Excessive testosterone can have negative effects on 20-30+ other hormones and neurotransmitters. My discussion of two of the most directly affected hormones:
In any case, if you can switch to short-acting TRT then your hormones operate closer to normal, reducing the risk of side effects. Short-acting testosterone includes nasal gels, buccal troches and possibly certain oral formulations. The former two are the best proven, but are less convenient. A trial could at least establish whether the approach is helpful to you. These forms of TRT are simpler than trying to directly replace the suppressed GnRH with gonadorelin and the suppressed kisppeptin with kisspeptin-10.
Read some other accounts of the misery caused by excessive TRT dosing:
Especially this one:
But that begs the question.
I'm on 110mg of cyp a week right now.
Putting my total at trough around 700-750, and my free T at the upper end of the range.
If I half my dose. What's the point of being on TRT?
Most that get on T, are looking to get to the upper end of the normal range.
I was making between 200-300 total T, before TRT. Why would I half the dose to go down there again?
Maybe I should just come off and see if I can get my low natural going again.
If i half my dose. I'm sure my total T will drop below 500 or so.
The point of being on TRT is to treat hypogonadism and thereby improve overall health. If you had started with above-borderline natural free testosterone then most likely there would have been no point in being on TRT. The high-dose apologists may point to some rare conditions where functional hypogonadism exists in spite of seemingly normal testosterone levels. However, these are so uncommon that I don't think I've encountered a single documented case in the forums.
In any case, because you were hypogonadal originally, successful treatment does not require high-end trough testosterone and supraphysiological peaks. This is simply asking for side effects. What you're looking for is the level/variation in levels that gives you the best results overall. This is likely going to be in the physiological range—maybe in the vicinity of your healthy youthful levels—and low-and-slow dosing is a tried-and-true approach. While both dose increases and dose decreases can cause transient misleading effects, dose increases are usually more pleasant, and limiting the rate of increase minimizes spurious results.
That's because of the widespread more-is-better delusion surrounding testosterone. Sometimes it's encouraged by unscrupulous doctors, but more charitably doctors are often responding to patient demand.
If enhanced musculature and athleticism is a priority over general health then more testosterone is indeed better. But let's not pretend that such dosing is TRT.
You're looking to have heathy levels. Naturally occurring morning total testosterone of 200-300 ng/dL implies low free testosterone and hypogonadism unless you had rock-bottom SHBG. Having a trough testosterone around 500 ng/dL on TRT is still a gigantic increase. TRT peaks on two injections per week are likely to be at least 40-50% higher than troughs, e.g. 700-800 ng/dL. Don't think for a moment that these levels are not worth trying. In my opinion, such levels should have been tried at the start, not as a fall-back after having problems with excess.
At this point I am willing to try anything. I'll try slowly lowering the dose and see if any changes.
I had exactly the same issue as you. I tried everything, and in the end it was solved simply by taking Proviron or by using scrotal testosterone cream with a lower dose of cypionate (a hybrid protocol). Both approaches substantially raise DHT. Proviron not necessarily on serum labs, but through its effect as a methylated DHT. I need e2 mid range and DHT high/slightly supra to be optimal with sexual function, HCG is a must for me aswell.
Joe Sixpack
Active Member
Same here. T cream + cypionate injections + HCG. I felt suboptimal in many ways before implementing testosterone cream
What are you guys using for doses? with the cream and cyp injections?
What did the cream bring back that you were missing?
Thanks for the reply
Update here.
My urologist started be on cabergoline? at .5 mg twice a week. It mimics dopamine and I have seen a pick of in sensitive and libido. So it appears to be at least somewhat a dopamine/neurotransmitter issue. Has anyone used this long term? I also have selegine on hand, anybody combine these at low doses? What I don't understand is why my sensitivity and orgasm was fine pre-trt and why it gets blunted when on TRT when test is suppose to increase dopamine? Any thoughts?
My urologist started be on cabergoline? at .5 mg twice a week. It mimics dopamine and I have seen a pick of in sensitive and libido. So it appears to be at least somewhat a dopamine/neurotransmitter issue. Has anyone used this long term? I also have selegine on hand, anybody combine these at low doses? What I don't understand is why my sensitivity and orgasm was fine pre-trt and why it gets blunted when on TRT when test is suppose to increase dopamine? Any thoughts?
BadassBlues
Well-Known Member
I have used Cabergoline in the past with fairly good results. It tends to diminish however as receptor sensitivity declines. It's best to cycle it.
I would definitely not mix Selegeline and Cabergoline.
I've been on Cabergiline for about five years. I started at the standard dose of 0.5mg twice a week and went up to 3× week. Does it help? I have no idea. I'm throwing everything I can at the problem and I don't know what works and what doesn't but I'm not going to stop any of these modalities lest it be the one thing that works - or even slightly helps. Anorgasmia is a XXXXX.
Phil Goodman
Well-Known Member
Don’t have any personal experience with caber so I ran it through an LLM to recap the approaches attempted so far along either results of each test. Received this:
So he’s at 110 mg/week total (≈55 mg 2×/week), which is a very reasonable, even conservative TRT dose. That makes the “too much testosterone → desensitization” explanation much less likely.
Let’s recalibrate based on that.
What the corrected dose implies
At 110 mg/week:- He’s likely in a mid–upper normal physiological range, not supraphysiologic
- Receptor downregulation from excess androgens is unlikely to be the main driver
Most plausible root causes (given his response pattern)
1) Neurosteroid deficiency (still the #1 suspect)
Even at normal TRT doses, shutdown of the testes reduces:- pregnenolone
- allopregnanolone
- DHEA
- genital sensitivity
- orgasm intensity
- CNS sexual reward
- HCG → partial improvement
- THC → better orgasm
2) Dopamine signaling issue — but specifically receptor-level
The biggest clue in the entire post is this:- Wellbutrin → no effect
- Cabergoline → noticeable improvement
It’s not dopamine availability
It’s dopamine receptor activation/sensitivity
Cabergoline directly stimulates D2 receptors → bypasses upstream issues
So the problem is likely:
- reduced receptor sensitivity
- altered downstream signaling
3) Prolactin dynamics (not baseline level)
He said:That’s normal—but misleading.
What matters more:
- post-orgasm prolactin spikes
- dopamine ↔ prolactin balance
4) Peripheral sensitivity (penile nerve response)
This part is often dismissed, but his symptom is very specific:That’s a mechanical sensory threshold issue, not just libido.
Possible contributors:
- reduced DHT effect locally
- altered nerve sensitivity
- CNS filtering of sensory input
What his trial-and-error already ruled out
He actually did a solid job testing variables:Likely NOT the main issue:
- Estrogen (wide range tested, no change)
- Basic dopamine deficiency (tyrosine, Wellbutrin failed)
- Severe prolactin elevation
- Pure erectile dysfunction (he can get/maintain erection without condom)
About his current approach (this matters)
Cabergoline
Yes, it helped—but:- it’s a powerful D2 agonist
- long-term use is not benign
- impulse control issues
- emotional flattening
- cardiac valve risk (dose-dependent but real)
Selegiline
Stacking this with cabergoline is where things can get sketchy:- increases dopamine tone further
- can overshoot into side effects
- still doesn’t address root cause
What I’d actually recommend (based on THIS scenario)
1) Keep TRT dose as-is (for now)
110 mg/week is reasonable.I would not lower it yet since:
- symptoms aren’t classic high-T issues
- problem seems more neurochemical than androgen excess
2) Optimize HCG (this is high-yield for him)
He saw partial benefit → that’s important.Instead of:
- 1000 IU/week inconsistently
- 250–350 IU, 3×/week (steady dosing)
- stabilize intratesticular function
- improve neurosteroid output
3) Trial neurosteroid support (very relevant here)
This is the missing piece in a lot of TRT protocols:- pregnenolone (start low, ~10–20 mg)
- possibly DHEA (if labs support)
- supports CNS sexual signaling
- can improve orgasm quality and sensitivity
4) Check DHT (don’t assume it’s fine)
Even on TRT, some men have:- relatively low DHT activity
- reduced penile sensitivity
- weaker orgasm
- that’s a cleaner fix than dopamine drugs
5) Avoid routine AI use
Even though he experimented with Arimidex:- AIs often worsen sexual experience
- serum E2 ≠ brain estrogen signaling
→ leave estrogen alone
6) Use cabergoline cautiously (if at all)
Given his response, it can be:- a diagnostic clue
- possibly a short-term tool
- a clear prolactin issue
- medical supervision
7) Don’t ignore the “condom effect”
What he described is actually common:- reduced sensitivity + condom = below arousal threshold
- leads to erection loss
Answer to his core confusion
Because TRT changes more than testosterone:
Before:
- full neurosteroid production
- natural dopamine cycling
- intact HPTA signaling
After:
- stable testosterone
- reduced neurosteroids
- altered dopamine/prolactin balance
- good erections
- worse experience
Bottom line
Given the corrected dose, the most likely stack of causes is:- Neurosteroid suppression (primary)
- Dopamine receptor-level changes
- Possible DHT / peripheral sensitivity component
@BadassBlues how do you cycle it?
@Mark7 are you having good results as far as libido and orgasm being normal or improved?
What else are you on?
Thank you for doing that. I'll look intoDon’t have any personal experience with caber so I ran it through an LLM to recap the approaches attempted so far along either results of each test. Received this:
So he’s at 110 mg/week total (≈55 mg 2×/week), which is a very reasonable, even conservative TRT dose. That makes the “too much testosterone → desensitization” explanation much less likely.
Let’s recalibrate based on that.
What the corrected dose implies
At 110 mg/week:
So now the strongest explanations become:
- He’s likely in a mid–upper normal physiological range, not supraphysiologic
- Receptor downregulation from excess androgens is unlikely to be the main driver
Most plausible root causes (given his response pattern)
1) Neurosteroid deficiency (still the #1 suspect)
Even at normal TRT doses, shutdown of the testes reduces:
These affect:
- pregnenolone
- allopregnanolone
- DHEA
Key supporting evidence from his post:
- genital sensitivity
- orgasm intensity
- CNS sexual reward
That combination strongly points to:
- HCG → partial improvement
- THC → better orgasm
2) Dopamine signaling issue — but specifically receptor-level
The biggest clue in the entire post is this:
That tells you:
- Wellbutrin → no effect
- Cabergoline → noticeable improvement
It’s not dopamine availability
It’s dopamine receptor activation/sensitivity
Cabergoline directly stimulates D2 receptors → bypasses upstream issues
So the problem is likely:
- reduced receptor sensitivity
- altered downstream signaling
3) Prolactin dynamics (not baseline level)
He said:
That’s normal—but misleading.
What matters more:
Cabergoline improving symptoms suggests:
- post-orgasm prolactin spikes
- dopamine ↔ prolactin balance
4) Peripheral sensitivity (penile nerve response)
This part is often dismissed, but his symptom is very specific:
That’s a mechanical sensory threshold issue, not just libido.
Possible contributors:
Again—THC helping supports sensory processing, not just hormones.
- reduced DHT effect locally
- altered nerve sensitivity
- CNS filtering of sensory input
What his trial-and-error already ruled out
He actually did a solid job testing variables:
Likely NOT the main issue:
- Estrogen (wide range tested, no change)
- Basic dopamine deficiency (tyrosine, Wellbutrin failed)
- Severe prolactin elevation
- Pure erectile dysfunction (he can get/maintain erection without condom)
Cabergoline
Yes, it helped—but:
Risks (even at moderate doses):
- it’s a powerful D2 agonist
- long-term use is not benign
- impulse control issues
- emotional flattening
- cardiac valve risk (dose-dependent but real)
Selegiline
Stacking this with cabergoline is where things can get sketchy:
This is moving toward “neurochemical brute force,” not restoration.
- increases dopamine tone further
- can overshoot into side effects
- still doesn’t address root cause
What I’d actually recommend (based on THIS scenario)
1) Keep TRT dose as-is (for now)
110 mg/week is reasonable.
I would not lower it yet since:
- symptoms aren’t classic high-T issues
- problem seems more neurochemical than androgen excess
2) Optimize HCG (this is high-yield for him)
He saw partial benefit → that’s important.
Instead of:
Try:
- 1000 IU/week inconsistently
Goal:
- 250–350 IU, 3×/week (steady dosing)
- stabilize intratesticular function
- improve neurosteroid output
3) Trial neurosteroid support (very relevant here)
This is the missing piece in a lot of TRT protocols:
Why:
- pregnenolone (start low, ~10–20 mg)
- possibly DHEA (if labs support)
- supports CNS sexual signaling
- can improve orgasm quality and sensitivity
4) Check DHT (don’t assume it’s fine)
Even on TRT, some men have:
Low DHT can cause:
- relatively low DHT activity
If low:
- reduced penile sensitivity
- weaker orgasm
- that’s a cleaner fix than dopamine drugs
5) Avoid routine AI use
Even though he experimented with Arimidex:
Unless there are strong symptoms:
- AIs often worsen sexual experience
- serum E2 ≠ brain estrogen signaling
→ leave estrogen alone
6) Use cabergoline cautiously (if at all)
Given his response, it can be:
But not something I’d rely on long-term without:
- a diagnostic clue
- possibly a short-term tool
- a clear prolactin issue
- medical supervision
7) Don’t ignore the “condom effect”
What he described is actually common:
This reinforces:
- reduced sensitivity + condom = below arousal threshold
- leads to erection loss
Answer to his core confusion
Because TRT changes more than testosterone:
Before:
- full neurosteroid production
- natural dopamine cycling
- intact HPTA signaling
After:
For some men, that tradeoff results in:
- stable testosterone
- reduced neurosteroids
- altered dopamine/prolactin balance
- good erections
- worse experience
Bottom line
Given the corrected dose, the most likely stack of causes is:
Cabergoline “working” doesn’t contradict that—it actually supports it.
- Neurosteroid suppression (primary)
- Dopamine receptor-level changes
- Possible DHT / peripheral sensitivity component
pregnenolone (start low, ~10–20 mg)
possibly DHEA (if labs support)
Phil Goodman
Well-Known Member
I use a pretty low dose of DHEA (12.5 mg/day) and think I’m more sensitive to it than most men. I occasionally take 25 mg/day for more energy, but when I do I inevitably have less sleep that night, around 6 hours when I usually hit between 7-8.
Whenever I try pregnenolone my well-being always takes a hit around 4-5 days in and I never make it past 7. That’s on 25 mg/day though, so perhaps I’d do better on 10 and/or by pushing through and letting my body adjust. But I don’t really have any issues and have done it more experimentally to see if it would provide added benefits… but again I end up stopping around the one week mark. If you start at 10 you should minimize the likelihood of that situation though.
BadassBlues
Well-Known Member
Being a D2 receptor agonist, Cabergoline starts working within a few hours. We are discussing an "Off Label" usage, so the parameters used for treating Prolactinomas and Parkinsons aren't the same. Peak plasma concentrations are between 1-2 hours; you will notice the effects very quickly. The half-life is around 70 hours (which is why the twice weekly protocol). The effects do get a little better the following days after initial dosing.
So, this being the case you could potentially use this on an "as needed" basis. Take it on Thursday for a weekend getaway, do 3 weeks on and take a week off, or 2 weeks on and 2 weeks off.
There are multiple options. The thing you want to do is give your D2 receptors a break so as to maintain normal function.
I got to where I was just using it on demand. The downside to Cabergoline (and all D2 receptor agonists) is the grogginess that they cause. Caber is definitely better than the rest, but it still has similar side effects.
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