In my quest to conquer ED, I have tried and reported here on my experience with Vyleesi branded, PT 141 (EM power), Tri Mix, Quad Mix, Botox, PRP injections (P Shot), Shockwave ( a real clinic quality system given by an experienced physician). One of the benefits of being treated by an experienced, well trained doc for ED is their knowledge of the meds, and how and when and where they can push the dosing for better benefits. She started me on 5 mg once a day of tadalafil. At her suggestion, the dose increased to 10 mg a day. About 6 months or so ago, we increased the dose to 15 mg, because I kept seeing benefit, with increasing doses. Each increase in dose saw the same side effects come back each time. For me, slight headache, and nasal congestion, and a little flushing. However, after each dose, I saw an increase in ease to get erections, easier ability to keep an erection and better sensitivity. And, after a relatively short time, the side effects dissipated. Recently we increased the dose yet again, to 20 mg per day. Thats a high dose of tadalafil. However, the jump in benefit this time was very significant. Yes, I did see the same side effects come back. Nasal congestion, headache, predominately. But it's now been about a week, and the side effects are largely gone. No more heachaches, nasal congestion is taking less and less time to resolve on its own. Now it comes on when the dose is probably absorbed and at full effect, but only lasts about a half hour or less. The biggest takeaway on effectiveness, has been a very significant increase in ability to get erections and ease in keeping them. I have also seen a very nice increase again in sensitivity. The takeaway here, is once you are acclimated to a medication like this, if you saw improvement but are not where you want/need to be, it is worth the conversation with your doc about increasing the dose. I was concerned about the high dose, however, she reminded me the dosing for pulmonary hypertension (tadalafil is approved and effective for treating pulmonary hypertension) STARTS at 20mg and goes up to 40 mg. So we know it can be taken safely at these doses. It is a relatively inexpensive option for those who have ED issues and worth investigating going up in dose if you are not where you want to be. The KEY it seems for me, was to gradually increase the dose.
Increasing doses of Tadalafil
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Fernando Almaguer
Well-Known Member
how old are you if you don't mind me asking?
65. My protocol is 50-56mg TC EOD and HCG 500iu every third day.
Golfboy307
Active Member
In the last few months, I nudged my daily dose from 5mg to around 7mg which resulted in a large noticeable difference. I feel like the key as we get older is to maintain the quality of our arterial lining (the best we can) so these drugs don't lose effectiveness. That is my goal at least.
Systemlord
Member
Increasing the dose of Cialis works fine so long as it doesn’t lower your estrogen too much. This is not guaranteed to happen to everyone.
My estrogen got knocked down to 18 pg/mL on 2.5 mg with medium body fat percentage and a 592 ng/dL midpoint level and 1000+ ng/dL peak level.
Testosterone:estradiol ratio changes associated with long-term tadalafil administration: a pilot study - PubMed
Sustained improvement in sexual function after 12 months of tadalafil administration is associated with increased T:E ratio mainly related to reduction of E levels. We hypothesize that androgen-estrogen cross-talk and possible inhibition of aromatase activity during chronic exposure to tadalafil...
pubmed.ncbi.nlm.nih.gov
Fernando Almaguer
Well-Known Member
so you are totaling over 200 mg per week with test, correct?
Fernando Almaguer
Well-Known Member
What negatives did you notice from that, still getting erections with the medication?Increasing the dose of Cialis works fine so long as it doesn’t lower your estrogen too much. This is not guaranteed to happen to everyone.
My estrogen got knocked down to 18 pg/mL on 2.5 mg with medium body fat percentage and a 592 ng/dL midpoint level and 1000+ ng/dL peak level.
Testosterone:estradiol ratio changes associated with long-term tadalafil administration: a pilot study - PubMed
Sustained improvement in sexual function after 12 months of tadalafil administration is associated with increased T:E ratio mainly related to reduction of E levels. We hypothesize that androgen-estrogen cross-talk and possible inhibition of aromatase activity during chronic exposure to tadalafil...
Yes, there about. I'm feeling well and my Ft is 29.8 and Estradiol 40.8. That was at the 50mg EOD.
phalloguy100
Active Member
Wait, cialis can lower estrogen levels?!! No wonder I stopped needing arimidex!!Increasing the dose of Cialis works fine so long as it doesn’t lower your estrogen too much. This is not guaranteed to happen to everyone.
My estrogen got knocked down to 18 pg/mL on 2.5 mg with medium body fat percentage and a 592 ng/dL midpoint level and 1000+ ng/dL peak level.
Testosterone:estradiol ratio changes associated with long-term tadalafil administration: a pilot study - PubMed
Sustained improvement in sexual function after 12 months of tadalafil administration is associated with increased T:E ratio mainly related to reduction of E levels. We hypothesize that androgen-estrogen cross-talk and possible inhibition of aromatase activity during chronic exposure to tadalafil...
BadLeroyBrown
New Member
Same thing here once I bumped my Tadalafil up to 10mg most days (once or twice a week on my rest days I will only take 5mg) my constantly rising E2 that I would usually take .125mg of Anastrozle twice a week for subsided enough to stop taking the AI. Now I only use .125mg of Anastrozole every now and then if I look and feel like I'm retaining water and crying while watching the Gilmore Girls. I mean for the record I don't watch Gilmore Girls, its my daughters who watch it guys...I swear!
Systemlord
Member
As it turns out I was never experiencing symptoms of low-T, at a total testosterone of 120, as unbelievable as that sounds. My symptoms were coming solely from the obesity and type 2 diabetes.
Yes my testosterone is low on paper, but this is normal for me and newly discovered normal for my father. My father told me his testosterone levels were checked in his 70's his doctor told him his levels were very low and took no action because his was asymptomatic.
Cialis cause me intense hot flashes, like I'm on fire. I don't need ED drugs.
Systemlord
Member
Testosterone:estradiol ratio changes associated with long-term tadalafil administration: a pilot study - PubMed
Sustained improvement in sexual function after 12 months of tadalafil administration is associated with increased T:E ratio mainly related to reduction of E levels. We hypothesize that androgen-estrogen cross-talk and possible inhibition of aromatase activity during chronic exposure to tadalafil...
pubmed.ncbi.nlm.nih.gov
Fernando Almaguer
Well-Known Member
I was in the mid 300s and had no ED maybe I didn't need it either. Now 8 years in I fear coming off. Although It has helped me in other areas like confidence, muscle mass, ability to train hard and recover, cognition... I wonder if Ill ever know what 300 TT feels like again. Im glad you got your diabetes and obesity figured out. what's the story on that? how did you fix it?Testosterone:estradiol ratio changes associated with long-term tadalafil administration: a pilot study - PubMed
Sustained improvement in sexual function after 12 months of tadalafil administration is associated with increased T:E ratio mainly related to reduction of E levels. We hypothesize that androgen-estrogen cross-talk and possible inhibition of aromatase activity during chronic exposure to tadalafil...
phalloguy100
Active Member
Random question here… but has anyone tried Cialis AND Flomax together? Flomax is sometimes given for BPH or kidney stones on people who also happen to be on cialis for ED. I wonder if together they help ED even more since flomax can cause erections and some folks say it gives them a lower flaccid hang.
I currently take terazosin 2 mg bid for BP control and to help with bph symptoms, along with the higher doses of Tadalafil now up to 40 mg per day. I don’t have E issues, and the Tadalafil works better and better as I went up in dose. A huge improvement. The terazosin is helpful, but I think it did more before I took the Tadalafil dose up.
madman
Super Moderator
Of course as they are both vasodilators mind you the vasodilating effects are less common with tamsulosin.
Doxazosin and terazosin would be your best bet!
Also need to keep in mind α1-blockers can cause ejaucalatory disorder (absent or reduced seminal fluid).
Key points here:
*Tissue distribution, subtype selectivity, and pharmacokinetic profiles of certain formulations may contribute to the tolerability profile of specific drugs. The most frequent adverse events of α1-blockers are asthenia, dizziness and (orthostatic) hypotension. Vasodilating effects are most pronounced with doxazosin and terazosin and are less common with alfuzosin and tamsulosin [168]. Patients with cardiovascular co-morbidity and/or vaso-active co-medication may be susceptible to α1-blocker-induced vasodilatation [169].
*The combination of α-blockers and PDE5Is versus α-blockers monotherapy leads to greater improvements in LUTS, QoL, erectile function and Qmax without increase in AEs.
*A SR concluded that α1-blockers do not adversely affect libido, or erectile function (ED), but can cause abnormal ejaculation (OR: 7.53) [176].
*In the meta-regression, the occurrence of EjD was independently associated with the improvement of urinary symptoms and flow rate, suggesting that the more effective the α1-blocker is the greater the incidence of EjD.
*Sexually active patients treated with selective α1-blockers should be counselled about the risk of EjD.
5.6.3.6 Safety concerns for PDE5Is
5.6.3.6.4 Interactions with α-blockers
Tadalafil 5 mg is currently the only licensed drug for the treatment of both ED and LUTS demonstrating overall good efficacy in relieving urinary symptoms and improving EF [367]. Therefore, treatment with tadalafil 5 mg should be considered in patients suffering from mild to moderate LUTS associated with ED either alone or in combination with α-blockers. Conversely, as both drugs are vasodilators a certain degree of caution has been observed for combination therapy with PDE5Is and alpha-blockers due to the potential cumulative effects on blood pressure described in some studies [361, 369, 387]. However, a meta-analysis concluded that a concomitant treatment with α-blockers [both non-uroselective (e.g., terazosin and doxazosin) and uro-selective(e.g., alfuzosin, tamsulosin and silodosin] and PDE5Is may produce changes in haemodynamic parameters, but it does not increase the rate of adverse events due to hypotension [387]. Therefore, there is no current limitationi n the simultaneous use of α-blockers and PDE5I.
EAU Guidelines on Non-Neurogenic Male Lower Urinary Tract Symptoms (LUTS) 2024
5.2 Pharmacological treatment
5.2.1 α1-Adrenoceptor antagonists (α1-blockers)
Mechanism of action: α1-blockers aim to inhibit the effect of endogenously released noradrenaline on smooth muscle cells in the prostate and thereby reduce prostate tone and BOO [155]. However, α1-blockers have little effect on urodynamically determined bladder outlet resistance [156], and treatment-associated improvement of LUTS correlates poorly with obstruction [157]. Thus, other mechanisms of action may also be relevant.
Alpha 1-adrenoceptors located outside the prostate (e.g. urinary bladder and/or spinal cord) and α1-adrenoceptor subtypes (α1B- or α1D-adrenoceptors) may play a role as mediators of effects. Alpha1-adrenoceptors in blood vessels, other non-prostatic smooth muscle cells, and the central nervous system may mediate adverse events.
Currently available α1-blockers are: alfuzosin hydrochloride (alfuzosin); doxazosin mesylate(doxazosin); silodosin; tamsulosin hydrochloride (tamsulosin); terazosin hydrochloride (terazosin); and naftopidil. Alpha 1-blockers exist in different formulations. Although different formulations result in different pharmacokinetic and tolerability profiles, the overall difference in clinical efficacy between the difference formulations seems negligible.
Efficacy: Indirect comparisons and limited direct comparisons between α1-blockers demonstrate that allα1-blockers have a similar efficacy in appropriate doses [158]. Clinical effects take a few weeks to develop fully, but significant efficacy over placebo can occur within hours to days [157].
Controlled studies show that α1-blockers typically reduce IPSS by approximately 30-40% and increase Qmax by approximately 20-25%. However, substantial improvements also occurred in the corresponding placebo arms [63, 159]. In open-label studies, an IPSS improvement of up to 50% and Qmax increase of up to 40% were documented [63, 159]. A SR and meta-analysis suggested that Qmax variation underestimates the real effect of α1-blockers on BPO, as small improvements in Qmax correspond to relevant improvements in BOO index in PFS [160].
Alpha 1-blockers can reduce both storage and voiding LUTS. Prostate size does not affect α1-blocker efficacy in studies with follow-up periods of less than one year, but α1-blockers do seem to be more efficacious in patients with smaller prostates (< 40 mL) in longer-term studies [65, 161-164]. The efficacy of α1-blockersis similar across age groups [159]. A pooled analysis of phase III and IV trials of silodosin 8 mg demonstrated that improvements in total, storage, voiding, and QoL IPSS scores were similar for the severe and not severe LUTS cohorts [165]. In addition, α1-blockers neither reduce prostate size nor prevent AUR in long-term studies[162-164]; however, evidence suggests that the use of α1-blockers (alfuzosin, tamsulosin and silodosin) improve resolution of AUR [166, 167]. Nonetheless, IPSS reduction and Qmax improvement during α1-blocker treatment appears to be maintained over at least four years
Tolerability and safety: Tissue distribution, subtype selectivity, and pharmacokinetic profiles of certain formulations may contribute to the tolerability profile of specific drugs. The most frequent adverse events of α1-blockers are asthenia, dizziness and (orthostatic) hypotension. Vasodilating effects are most pronounced with doxazosin and terazosin and are less common with alfuzosin and tamsulosin [168]. Patients with cardiovascular co-morbidity and/or vaso-active co-medication may be susceptible to α1-blocker-induced vasodilatation [169]. In contrast, the frequency of hypotension with the α1A-selective blocker silodosin is comparable with placebo [170]. In a large retrospective cohort analysis of men aged > 66 years treated with α1-blockers the risks of falling (odds ratio [OR] 1.14) and of sustaining a fracture (OR 1.16) was increased, most likely as a result of induced hypotension [171]. In terms of cardiovascular risk, a large population-based study reported an increased risk of cardiac failure with long-term α-blocker use (HR 1.22), which was higher for non selective α-blockers [172]. Whilst there has been concern about a possible risk of dementia with long-term use of α1-blockers, a large Finnish nationwide case-control study of 24,602 cases and 98,397 controls did not find evidence of a significant association [173].
An adverse ocular event termed intra-operative floppy iris syndrome (IFIS) was reported in 2005, affecting cataract surgery [174]. A meta-analysis on IFIS after alfuzosin, doxazosin, tamsulosin or terazosin exposure showed an increased risk for all α1-blockers [175]. However, the OR for IFIS was much higher for tamsulosin. It appears prudent not to initiate α1-blocker treatment prior to scheduled cataract surgery, and the ophthalmologist should be informed about α1-blocker use.
A SR concluded that α1-blockers do not adversely affect libido, or erectile function (ED), but can cause abnormal ejaculation (OR: 7.53) [176]. Originally, abnormal ejaculation was thought to be retrograde, but more recent data demonstrate that it is due to a decrease or absence of seminal fluid during ejaculation, with young age being an apparent risk factor. In a meta-analysis ejaculatory dysfunction (EjD) was significantly more common with α1-blockers than with placebo (OR: 5.88). In particular, EjD was significantly more commonly related with tamsulosin or silodosin (OR: 8.57 and 32.5) than placebo, while both doxazosin and terazosin (OR:0.80 and 1.78) were associated with a low risk of EjD [177]. In the meta-regression, the occurrence of EjD was independently associated with the improvement of urinary symptoms and flow rate, suggesting that the more effective the α1-blocker is the greater the incidence of EjD.
Practical considerations: α1-blockers are usually considered the first-line drug treatment for male LUTS because of their rapid onset of action, good efficacy, and low rate and severity of adverse events. However, α1-blockers do not prevent occurrence of urinary retention or need for surgery. Ophthalmologists should be informed about α1-blocker use prior to cataract surgery. Elderly patients treated with non-selective α1-blockers should be informed about the risk of orthostatic hypotension. Sexually active patients treated with selective α1-blockers should be counselled about the risk of EjD.
5.2.5 Phosphodiesterase 5 inhibitors
Mechanism of action: Phosphodiesterase 5 inhibitors (PDE5Is) increase intracellular cyclic guanosine monophosphate, thus reducing smooth muscle tone of the detrusor, prostate, and urethra. Nitric oxide and PDE5Is might also alter reflex pathways in the spinal cord and neurotransmission in the urethra, prostate, or bladder [249]. Moreover, chronic treatment with PDE5Is seems to increase blood perfusion and oxygenation in the LUT [250]. Phosphodiesterase 5 inhibitors could also reduce chronic inflammation in the prostate and bladder [251]. The exact mechanism of PDE5Is on LUTS remains unclear.
5.2.7.4 α1-blockers + Phosphodiesterase 5 inhibitors
Mechanism of action: Combination treatment consists of an α1-blocker together with a phosphodiesterase 5 inhibitor (Section 5.2.5) with the intent to achieve better improvements in LUTS.
Efficacy: A meta-analysis of five RCTs (two studies with tadalafil 20 mg daily, two with sildenafil 25 mg, and one with vardenafil 20 mg), showed that combination therapy significantly improved IPSS score (-1.8), IIEF score (+3.6) and Qmax (+1.5 mL/s) compared with α-blockers alone [255]. Both a SR and Cochrane review found similar findings, and a network meta-analysis of 55 RCTs (excluding 5-ARIs) found that the combination of PDE5Is andα-blockers had greater IPSS improvement than monotherapy and any other combination therapy [253, 313, 314].These results have been confirmed by prospective studies which have shown an improvement in the IPSS QoL,IIEF-5 score and Qmax in patients taking PDE5Is and α-blockers [252, 315].
Tolerability and safety: No serious AEs have been reported in the association of PDE5-Is and α-blockers. In RCT comparing α-blockers alone with combined therapy, AEs occur with similar incidence across the two treatments arms suggesting that the addition of PDE5Is to α-blockers is well tolerated [316].
Practical consideration: The combination of α-blockers and PDE5Is versus α-blockers monotherapy leads to greater improvements in LUTS, QoL, erectile function and Qmax without increase in AEs. Data from meta-analyses suggest how younger men with low body mass index and more severe LUTS may be the population that benefits most from this association [255]. However, further studies with large populations and longer follow-up are needed to confirm these findings.
madman
Super Moderator
Driving down ones estradiol is not a given when using on demand or daily tadalafil.
Never put a dent in my estradiol!
Everyone so caught up on that study!
phalloguy100
Active Member
I think it did for me… Even when I increased hcg, my E2 still didn’t go up much. That was about the same time I started daily cialis.
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