TRT and Finasteride?

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I may be stupid but I have a question. If you are on TRT and your DHT is high why wouldn’t you merely lower your testosterone dose? I’m fairly certain that most of the benefits of testosterone require that it first be converted to DHT, the exception being muscles, which use testosterone directly. So, a man has low testosterone and along with it low DHT and the resulting low libido and erectile disfunction. He injects testosterone which converts to DHT so that it can be used to stimulate the libido and cause erections. His DHT is high due to the testosterone injections so he takes finasteride to lower DHT, the very thing that was low to begin with. It makes more sense to me to monitor the DHT level and adjust the testosterone dose accordingly rather than inject too much testosterone then take a drug to counteract its effects.
 
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M
You must be one of the clowns from the bro forums that hold a grudge.....almost as bad as the manchild who lurks on here!

Let me put it plain and simple numbskull...the metabolites estradiol and DHT are needed in healthy amounts to experience the full spectrum of testosterones beneficial effects.

Mood, energy, libido, erectile function, cardiovascular/brain/bone/immune system health, body composition.

*Considerable evidence exists in the contemporary literature regarding the physiological role of 5a-reductases in the peripheral tissues and CNS and the pathophysiological implication of inhibiting this family of enzymes and blunting biosynthesis of neurosteroids, which are critical biological mediators in the CNS, and contribute to altered mood, cognition, and libido (23–50). Also, significant pre-clinical evidence exists demonstrating that inhibition of 5a-RIs contributes to erectile dysfunction (16–22) and may also contribute to neurological symptoms (Fig. 4 (36).




Let's dig a Lil deeper champ!


DISCUSSION

Until recently, the adverse effects of finasteride and dutasteride therapy on sexual function were not recognized or well understood. However, a body of emerging evidence suggests that the assessment of sexual side effects of finasteride in many clinical studies was not accurately captured or reported (83). In addition, considerable bias and inaccuracies in reporting adverse effects of finasteride or dutasteride in most clinical trials of men AGA (83). An editorial following the report by Belknap (83) highlighted the need to re-think the safety of these drugs (188).

It is not surprising that almost all studies published to date do report increased sexual adverse effects. However, even when such sexual adverse events were reported, many argued that the numbers of subjects afflicted are small and propagated the falsehood that the adverse effects do resolve with continued treatment. This is unfortunately willful blindness and a deceptive method to continue to prescribe these drugs to unsuspecting young men. The number of subjects experiencing adverse events is neither small nor irrelevant, given the persistent nature of adverse events in susceptible individuals. For those individuals afflicted, this constitutes a life sentence of sexual dysfunction, depression, and/or anxiety. To put this in perspective, approximately 30 million young men, worldwide, would be prescribed finasteride or dutasteride treat male pattern hair loss. Even if the incidence of persistent sexual adverse events is 3% to 5%, which may be viewed as a small number, approximately 900,000 to 1.5 million men would suffer persistent sexual and psychiatric adverse events. By no means this would be considered a small number and should not be dismissed or ignored.

The key argument raised by many clinicians remains:
What is the level of evidence supporting the persistent nature of the sexual adverse effects and psychological symptoms caused by finasteride?

Considerable evidence exists in the contemporary literature regarding the physiological role of 5a-reductases in the peripheral tissues and CNS and the pathophysiological implication of inhibiting this family of enzymes and blunting biosynthesis of neurosteroids, which are critical biological mediators in the CNS, and contribute to altered mood, cognition, and libido (23–50). Also, significant pre-clinical evidence exists demonstrating that inhibition of 5a-RIs contributes to erectile dysfunction (16–22) and may also contribute to neurological symptoms (Fig. 4 (36).


*Data from several studies as well as from the manufacturer own reporting that some adverse events do not resolve and may persist. A number of studies discussed in this review demonstrated that not all adverse events resolve with drug discontinuation and in some cases, they persist or become irreversible (8,12, 13, 52–54, 83, 84, 88, 67, 68, 115, 127, 129, 130, 170, 186–189). For these reasons, we find the argument that sexual adverse events resolve with continued treatment is outright inaccurate and, at best, deceptive.


The increased reporting of and documentation of persistent side effects in the clinical literature resulted in warnings by the Medicine Health Care Products Regulatory Agency (MHRA) public assessment report on the risk of finasteride published in December of 2009 in Section 4.8 Undesirable Effects, it was stated, ‘‘In addition, the following have been reported in post-marketing use: persistence of ED after discontinuation of treatment with PROPECIA.’’ Clearly, the sexual adverse events do not necessarily resolve completely in all patients, who discontinue use of finasteride, again supporting the premise that in some patients these sexual side effects remain ‘‘persistent.’’ Furthermore, in December 2008, the Swedish Medical Products Agency concluded its safety investigation of Propecia. The Agency's updated safety information now lists as a possible side-effect difficulty in obtaining an erection that persists even after discontinuing Propecia. In addition, in 2011, the USA FDA mandated that labeling of finasteride includes information about potential risks of depression as well as sexual dysfunction and problems and high-grade prostate cancer. In 2017, the European Medical Agency recommended adding depression and suicidal ideation to the finasteride label.

One other argument consistently made in the literature is that the low-quality evidence available does not support a causal link between finasteride and persistent symptoms. Examining the contemporary clinical literature, it appears that almost all studies published to date (Tables 1–3) demonstrated the increased onset of sexual dysfunction and psychiatric dysfunction, irrespective of the assessment method, age, or drug dose. How could such evidence be totally ignored and dismissed as low-quality evidence? Given that considerable level of bias is introduced in many of these studies since a large number of these clinical trials were funded and administered by the drug manufacturers, it is paramount that clinicians do their due diligence and not fall for the slogan, ‘‘these drugs are well-tolerated and safe.’’

It is imperative that we consider how safety reporting of adverse events due to finasteride and dutasteride have been inadequate in most clinical trials (83, 84). Indeed, this inaccurate reporting of harm makes the evidence regarding the adverse events to be limited and may appear of poor quality. Given the level of bias due to conflict of interest, it is not surprising that the level of harm is tampered down significantly. Well-trained and experienced clinicians may see the coexistence of adverse events as a distinct syndrome with its own pathogenesis rather than a simple random or haphazard co-occurrence. Despite the lack of final proofs, the presence of severe and persistent side effects induced by these drugs raises serious concerns for clinicians. Simply, a low estimated prevalence of PFS should not be used as an excuse for non-vigilance, given that these drugs are prescribed for millions of relatively young healthy men.
My female GP just told me she won’t test me for E2 because it’s a female hormone.
Welcome to Australia’s medical world for idiots
 
M

My female GP just told me she won’t test me for E2 because it’s a female hormone.
Welcome to Australia’s medical world for idiots

My female GP once said testosterone doesn't affect muscle mass, it makes a men feel like a man. I whipped out my phone and asked Siri, "what does testosterone do for the male body", and was met by complete silence afterwards.
 
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My GP once said testosterone doesn't affect muscle mass, it makes a men feel like a man. I whipped out my phone and asked Siri, "what does testosterone do for the male body", and was met by complete silence afterwards.
A good GP’s great, but they’re few and far between these days because you make more money once you specialize, and GP’s don’t get to decide most of what they do, insurance algorithms basically do. That’s lead to horrible quality GP’s in most cases.

One of my friends got tested for his test twice. One time had the Total T at 125. The other time at 235 or so. Those are both below the normal range and the GP lady still said he’s fine.

Another lady I met recently has felt like crap for years, so I told her to have the usual tests done to see where she’s at hormonally. She said she had some of those done over the past few years, and for 3 years straight she had less E2 than I do. It even says right on the test that if it’s that low you need to retest again and there’s probably an issue there, but nobody said anything for years. I got her to go to a specialist and it’s still lower than my own E2. She also has a bulge on her thyroid and I told her to get her free T3 and 4 and TSH checked and the bulge and what do you know, issues there too, and she has cysts everywhere. After a cancer check she’s probably getting on HRT. She went 3+ years of feeling like complete garbage and blood tests showing why and her GPs said she was fine despite not even being in the normal range.

You could replace most GPs now with a post it note that says “You’re fine, but would you like some Xanax?“ and we’d get the same quality of care in the US in most places. I was surprised it happened to her too since girls usually get anything they want if they walk in with so much as a headache.
 
A good GP’s great, but they’re few and far between these days because you make more money once you specialize, and GP’s don’t get to decide most of what they do, insurance algorithms basically do. That’s lead to horrible quality GP’s in most cases.

One of my friends got tested for his test twice. One time had the Total T at 125. The other time at 235 or so. Those are both below the normal range and the GP lady still said he’s fine.

Another lady I met recently has felt like crap for years, so I told her to have the usual tests done to see where she’s at hormonally. She said she had some of those done over the past few years, and for 3 years straight she had less E2 than I do. It even says right on the test that if it’s that low you need to retest again and there’s probably an issue there, but nobody said anything for years. I got her to go to a specialist and it’s still lower than my own E2. She also has a bulge on her thyroid and I told her to get her free T3 and 4 and TSH checked and the bulge and what do you know, issues there too, and she has cysts everywhere. After a cancer check she’s probably getting on HRT. She went 3+ years of feeling like complete garbage and blood tests showing why and her GPs said she was fine despite not even being in the normal range.

You could replace most GPs now with a post it note that says “You’re fine, but would you like some Xanax?“ and we’d get the same quality of care in the US in most places. I was surprised it happened to her too since girls usually get anything they want if they walk in with so much as a headache.
Tell that lady with cysts to start taking iodine. Cysts are caused by lack of iodine. Sounds like she has a goiter on her thyroid, which is also caused by lack of iodine. Here’s a great lecture about iodine deificiency, goiters and cysts
 
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@SixHouse Have u looked into progesterone? As far as I know, progesterone lowers the conversion of testosterone into DHT by competing with testosterone at the 5ar enzyme. Most guys on TRT will have low progesterone levels due to the majority of progesterone, in males, being made by in the testicles. When testosterone shuts down the males testicles, usually most of their progesterone production gets shut down as well. I personally always test at the very bottom of the range for progesterone. Started taking injectable progesterone recently to get my levels back in the normal range

Also, checkout this video by Dr. Paul Saladino that he just released. I haven’t watched it yet, but the guys is literally a computer. Idk how he knows everything he knows, and retains all the knowledge that he has. Check it out tho, hopefully it has some info that can help u out
 
@SixHouse Have u looked into progesterone? As far as I know, progesterone lowers the conversion of testosterone into DHT by competing with testosterone at the 5ar enzyme. Most guys on TRT will have low progesterone levels due to the majority of progesterone, in males, being made by in the testicles. When testosterone shuts down the males testicles, usually most of their progesterone production gets shut down as well. I personally always test at the very bottom of the range for progesterone. Started taking injectable progesterone recently to get my levels back in the normal range

Also, checkout this video by Dr. Paul Saladino that he just released. I haven’t watched it yet, but the guys is literally a computer. Idk how he knows everything he knows, and retains all the knowledge that he has. Check it out tho, hopefully it has some info that can help u out
Have you noticed any benefit from bringing your progesterone levels up? Mine too are at the very bottom of range.
 
Have you noticed any benefit from bringing your progesterone levels up? Mine too are at the very bottom of range.
Not any benefits that I’m aware of. I’m currently taking 2mg of empowers injectable progesterone. Actually getting labs done in 2 hours, and should hopefully have the results soon. I’ll post them here when I do
 
Have you noticed any benefit from bringing your progesterone levels up? Mine too are at the very bottom of range.
Not really. No negatives tho, so gonna continue using it just to have piece of mind that my progesterone levels are in a healthy range.
 
think I was supposed to update this thread with my lab results. So been using 2mg of injectable progesterone for about 2 months now, always injected before bed subQ. Progesterone levels at 8:30am came back at 1.6 (0.0-0.5). The old reference range was (0.0-1.0). I’ve heard that anywhere between 0.8-1.2 is a good range for progesterone to be. So I dropped my dose down to 1.5mg every night before bed, and hoping it brings my levels to around 1.2. Gonna recheck my progesterone levels again in 4 weeks

No subjective differences good or bad noticed. At least none that I’m aware of
 
 
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