Beware of DHT

Sicillian

New Member
I Started low dose TRT in 2016 for mainly libido/erection issues but also had mood and concentration problems. Wasn't much successful and cortisol went too low so quit after 8 or 9 months. Then tried HCG which worked for about 2 months but then E got too high and it stopped working at all. From then onwards, I was just chasing symptoms by trying different stuff. Low dose TE, TP, AI's, Proviron and different herbs. I knew that DHT was crucial for libido but wasn't able to raise it in a balanced way with consistent results. Every time it would work for some days and go too high with low estrogen symptoms (teary eyes, low mood, libido crash etc.) To get out of that (androgenic) state I had to take progesterone and I could then take TE without above symptoms, but, in this (estrogenic) state, I still had very little desire plus erection problems. Then again, I would try an AI or zinc or Proviron with T or HCG for the next round.
My heart was fine with all of this until the fall of 2019. I had injected low dose TE and also taken Proviron. Then I also ingested some astragalus root powder. I later found on the net that this lowers progesterone and estrogen. Any way at around midnight I woke up with my heart really struggling. It felt like it was pumping oil or something. I rushed up to my room and took a 100 mg progesterone pill and in minutes heart spasms went away and I was able to sleep. Next morning I went to the hospital for ECG and it was fine although I felt tired the whole day. Even though I became very careful I nevertheless had more cardiovascular events a few months later (heart palps, shortness of breath, nausea etc.) and to my horror, the progesterone did not help but made it worse (by supposedly blocking E I think). I went to the hospital the ECG was again fine and they gave me a date for stress test. I was feeling fine on that day and the stress test was also ok. Later I also had an Echocardiogram (ultrasound of heart) and that was fine too except the doctor said my heart walls were slightly thicker but he didn't seem concerned at all. I never told any doctor of steroids or anything I had taken.
I have stopped all steroids/AI etc. It has become clear that anything that raises DHT causes an immediate cardiovascular event. Also anything that lowers E is bad, even heart healthy stuff like Pomegranate juice. If I drink it for 3 or 4 days I get pain in my chest. AI's are totally out of question. Even Boron has started to cause heart pain. Not sure why that is. May be because it lowers SHBG and frees up T/DHT?
Any thing that blocks DHT (without blocking E also) relieves my heart of the pain like Finasteride, Astaxanthin, Rosemary oil, Lavender oil etc. Estrogenic and Anti androgenic stuff is what my heart is screaming for and it is not because my DHT is high. I just cannot seem to tolerate even normal range. I am really stuck with apparently no way without sacrificing one (sex) for the other (heart) .
This is just a warning to anyone who is on AI's or is trying to raise his DHT. If you can, please get off it before your heart stops tolerating androgens. Google DHT and heart and you will find links. Testosterones beneficial effects on heart are caused by its conversion to Estrogen while its deleterious effects are caused by its conversion to DHT. Of course this will not be true for everyone but there is a good chance you will screw your heart like me. Look it up.
 

madman

Member
I Started low dose TRT in 2016 for mainly libido/erection issues but also had mood and concentration problems. Wasn't much successful and cortisol went too low so quit after 8 or 9 months. Then tried HCG which worked for about 2 months but then E got too high and it stopped working at all. From then onwards, I was just chasing symptoms by trying different stuff. Low dose TE, TP, AI's, Proviron and different herbs. I knew that DHT was crucial for libido but wasn't able to raise it in a balanced way with consistent results. Every time it would work for some days and go too high with low estrogen symptoms (teary eyes, low mood, libido crash etc.) To get out of that (androgenic) state I had to take progesterone and I could then take TE without above symptoms, but, in this (estrogenic) state, I still had very little desire plus erection problems. Then again, I would try an AI or zinc or Proviron with T or HCG for the next round.
My heart was fine with all of this until the fall of 2019. I had injected low dose TE and also taken Proviron. Then I also ingested some astragalus root powder. I later found on the net that this lowers progesterone and estrogen. Any way at around midnight I woke up with my heart really struggling. It felt like it was pumping oil or something. I rushed up to my room and took a 100 mg progesterone pill and in minutes heart spasms went away and I was able to sleep. Next morning I went to the hospital for ECG and it was fine although I felt tired the whole day. Even though I became very careful I nevertheless had more cardiovascular events a few months later (heart palps, shortness of breath, nausea etc.) and to my horror, the progesterone did not help but made it worse (by supposedly blocking E I think). I went to the hospital the ECG was again fine and they gave me a date for stress test. I was feeling fine on that day and the stress test was also ok. Later I also had an Echocardiogram (ultrasound of heart) and that was fine too except the doctor said my heart walls were slightly thicker but he didn't seem concerned at all. I never told any doctor of steroids or anything I had taken.
I have stopped all steroids/AI etc. It has become clear that anything that raises DHT causes an immediate cardiovascular event. Also anything that lowers E is bad, even heart healthy stuff like Pomegranate juice. If I drink it for 3 or 4 days I get pain in my chest. AI's are totally out of question. Even Boron has started to cause heart pain. Not sure why that is. May be because it lowers SHBG and frees up T/DHT?
Any thing that blocks DHT (without blocking E also) relieves my heart of the pain like Finasteride, Astaxanthin, Rosemary oil, Lavender oil etc. Estrogenic and Anti androgenic stuff is what my heart is screaming for and it is not because my DHT is high. I just cannot seem to tolerate even normal range. I am really stuck with apparently no way without sacrificing one (sex) for the other (heart) .
This is just a warning to anyone who is on AI's or is trying to raise his DHT. If you can, please get off it before your heart stops tolerating androgens. Google DHT and heart and you will find links. Testosterones beneficial effects on heart are caused by its conversion to Estrogen while its deleterious effects are caused by its conversion to DHT. Of course this will not be true for everyone but there is a good chance you will screw your heart like me. Look it up.

Dihydrotestosterone: Biochemistry, Physiology, and Clinical Implications of Elevated Blood Levels (2017)


ABSTRACT

Benefits associated with lowered serum DHT levels after 5a-reductase inhibitor (5AR-I) therapy in men have contributed to a misconception that circulating DHT levels is an important stimulus for androgenic action in target tissues (e.g., prostate).
Yet evidence from clinical studies indicates that intracellular concentrations of androgens (particularly in androgen-sensitive tissues) are essentially independent of circulating levels. To assess the clinical significance of modest elevations in serum DHT and the DHT/testosterone (T) ratio observed in response to common T replacement therapy, a comprehensive review of the published literature was performed to identify relevant data. Although the primary focus of this review is about DHT in men, we also provide a brief overview of DHT in women. The available published data are limited by the lack of large, well-controlled studies of long duration that are sufficiently powered to expose subtle safety signals. Nonetheless, the preponderance of available clinical data indicates that modest elevations in circulating levels of DHT in response to androgen therapy should not be of concern in clinical practice. Elevated DHT has not been associated with increased risk of prostate disease (e.g., cancer or benign hyperplasia) nor does it appear to have any systemic effects on cardiovascular disease safety parameters (including increased risk of polycythemia) beyond those commonly observed with available T preparations. Well-controlled, long-term studies of transdermal DHT preparations have failed to identify safety signals unique to markedly elevated circulating DHT concentrations or signals materially different from T. (Endocrine Reviews 38: 220 – 254, 2017).




ESSENTIAL POINTS

· Circulating levels of DHT in response to testosterone replacement therapy (TRT) do not correlate with those found in androgen-sensitive tissue (e.g., prostate, adipose, muscle) due to local regulatory mechanisms that tightly control intracellular androgen homeostasis.

· The modest increases observed in serum DHT and in the DHT/T ratio observed after TRT are unlikely to be a cause of clinical concern, particularly when viewed in the context of changes observed in these parameters for currently marketed T-replacement products and those under development for which DHT data are available.

· While well-controlled, long-term studies designed to specifically examine the effects of androgen exposure on risk for the prostate needs to be conducted, the current clinical database is relatively reassuring that circulating levels of androgens (or changes in such) apparently do not play as pivotal a role as once thought in the development of the prostate disease.

· Robust epidemiologic or clinical trial evidence of a deleterious DHT effect on CVD is lacking. There is some evidence that DHT therapy in men with CVD may improve clinical status—a finding that needs confirmation. Data from a longitudinal database of older normal (i.e., not hypogonadal) indicated an association between serum DHT and incident CV disease and mortality. Conversely, others have reported that higher DHT levels in older men were associated with decreased all-cause mortality and reduced ischemic heart disease mortality. Additional exploration in prospective, placebo-controlled intervention studies of TRT with CVD as the primary endpoint is needed to resolve the long-term effects of androgens on CVD risks.

· DHT does not play a substantive role in body composition compared to T under normal conditions. Thus, elevated levels of DHT in response to TRT are unlikely to appreciably impact lean or fat mass. Nonetheless, data from animals suggest a role for DHT in adipose tissue that inhibits biochemical pathways involved in lipid synthesis and promotes several transcripts associated with apoptosis of adipocytes. Whether these DHT-induced effects also occur in human adipose tissue remains an area for future study.

· There is very limited data available regarding DHT and its effects on cognition. Further research is needed, particularly in light of animal data where DHT positively modified synaptic structure and significantly delayed cognitive impairment in a well-regarded animal model for Alzheimer’s disease. · Recent data indicating that higher levels of DHT were inversely associated with insulin resistance and risk of diabetes merit further mechanistic investigation to understand whether this action is separate from that of T.





Do Increases in Circulating Levels of DHT Increase Risk of CVD?

Clinical data from DHT administration in supraphysiologic doses on CVD


*Effect of DHT treatment in men with CAD
*Effect of oral TU and resultant elevated DHT in hypogonadal men with CAD


Effects of DHT on various biomarkers of CVD risk
*Vasodilatory effects of DHT in animal models and effects on endothelial nitric oxide synthase (eNOS) generation
*Evidence of DHT-mediated inhibition of macrophage foam cell formation
*Effects of DHT therapy on human inflammatory biomarkers
*Effects of DHT on EPCs
*Effects of DHT on platelet aggregation and thrombosis




Effects of DHT on Various Other Biological Processes and Tissues
*Erythropoiesis
*Lipids
*Skin

*Body composition

-Impact of exogenous DHT therapy on body composition
-Effects of 5a-reductase inhibition therapy and BMD on body composition

*Metabolic syndrome and type 2 diabetes
*Sexual function
*5a-reductase deficiency
*Gynecomastia
*Cognition
*Telomere length




In summary, we have reviewed the evidence that slightly to moderately elevated DHT concentrations or an elevated DHT/T ratio during androgen therapy (most notably, TRT) are unlikely to pose either a higher risk or a unique risk compared with T. We acknowledge that the available published data are limited by the lack of large, well-controlled studies of the long duration that are sufficiently powered to expose subtle safety signals. Nonetheless, the preponderance of available clinical data leads to the conclusion that modest elevations in circulating levels of DHT in response to androgen therapy should not be of concern in clinical practice.
 

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madman

Member
Keep in mind that although testosterone metabolites estradiol and DHT play a critical role in libido/erections that there is much more involved than just testosterone, estradiol, dihydrotestosterone, prolactin.

Although having healthy hormones is essential.....libido/ED is multifactorial!
 

Sicillian

New Member
Interesting. What were the TRT protocols (doses & frequency) you tried?
Initially the regular TRT in 2016 was 35 mg twice a week. Higher doses didn't seem to help. After that HCG 500 iu twice a week for about 2 months. After that there was no fixed dose or frequency though the T dose was almost always very little (10 to 20 mg).
 

Sicillian

New Member
Dihydrotestosterone: Biochemistry, Physiology, and Clinical Implications of Elevated Blood Levels (2017)


ABSTRACT

Benefits associated with lowered serum DHT levels after 5a-reductase inhibitor (5AR-I) therapy in men have contributed to a misconception that circulating DHT levels is an important stimulus for androgenic action in target tissues (e.g., prostate).
Yet evidence from clinical studies indicates that intracellular concentrations of androgens (particularly in androgen-sensitive tissues) are essentially independent of circulating levels. To assess the clinical significance of modest elevations in serum DHT and the DHT/testosterone (T) ratio observed in response to common T replacement therapy, a comprehensive review of the published literature was performed to identify relevant data. Although the primary focus of this review is about DHT in men, we also provide a brief overview of DHT in women. The available published data are limited by the lack of large, well-controlled studies of long duration that are sufficiently powered to expose subtle safety signals. Nonetheless, the preponderance of available clinical data indicates that modest elevations in circulating levels of DHT in response to androgen therapy should not be of concern in clinical practice. Elevated DHT has not been associated with increased risk of prostate disease (e.g., cancer or benign hyperplasia) nor does it appear to have any systemic effects on cardiovascular disease safety parameters (including increased risk of polycythemia) beyond those commonly observed with available T preparations. Well-controlled, long-term studies of transdermal DHT preparations have failed to identify safety signals unique to markedly elevated circulating DHT concentrations or signals materially different from T. (Endocrine Reviews 38: 220 – 254, 2017).




ESSENTIAL POINTS

· Circulating levels of DHT in response to testosterone replacement therapy (TRT) do not correlate with those found in androgen-sensitive tissue (e.g., prostate, adipose, muscle) due to local regulatory mechanisms that tightly control intracellular androgen homeostasis.

· The modest increases observed in serum DHT and in the DHT/T ratio observed after TRT are unlikely to be a cause of clinical concern, particularly when viewed in the context of changes observed in these parameters for currently marketed T-replacement products and those under development for which DHT data are available.

· While well-controlled, long-term studies designed to specifically examine the effects of androgen exposure on risk for the prostate needs to be conducted, the current clinical database is relatively reassuring that circulating levels of androgens (or changes in such) apparently do not play as pivotal a role as once thought in the development of the prostate disease.

· Robust epidemiologic or clinical trial evidence of a deleterious DHT effect on CVD is lacking. There is some evidence that DHT therapy in men with CVD may improve clinical status—a finding that needs confirmation. Data from a longitudinal database of older normal (i.e., not hypogonadal) indicated an association between serum DHT and incident CV disease and mortality. Conversely, others have reported that higher DHT levels in older men were associated with decreased all-cause mortality and reduced ischemic heart disease mortality. Additional exploration in prospective, placebo-controlled intervention studies of TRT with CVD as the primary endpoint is needed to resolve the long-term effects of androgens on CVD risks.

· DHT does not play a substantive role in body composition compared to T under normal conditions. Thus, elevated levels of DHT in response to TRT are unlikely to appreciably impact lean or fat mass. Nonetheless, data from animals suggest a role for DHT in adipose tissue that inhibits biochemical pathways involved in lipid synthesis and promotes several transcripts associated with apoptosis of adipocytes. Whether these DHT-induced effects also occur in human adipose tissue remains an area for future study.

· There is very limited data available regarding DHT and its effects on cognition. Further research is needed, particularly in light of animal data where DHT positively modified synaptic structure and significantly delayed cognitive impairment in a well-regarded animal model for Alzheimer’s disease. · Recent data indicating that higher levels of DHT were inversely associated with insulin resistance and risk of diabetes merit further mechanistic investigation to understand whether this action is separate from that of T.





Do Increases in Circulating Levels of DHT Increase Risk of CVD?

Clinical data from DHT administration in supraphysiologic doses on CVD


*Effect of DHT treatment in men with CAD
*Effect of oral TU and resultant elevated DHT in hypogonadal men with CAD


Effects of DHT on various biomarkers of CVD risk
*Vasodilatory effects of DHT in animal models and effects on endothelial nitric oxide synthase (eNOS) generation
*Evidence of DHT-mediated inhibition of macrophage foam cell formation
*Effects of DHT therapy on human inflammatory biomarkers
*Effects of DHT on EPCs
*Effects of DHT on platelet aggregation and thrombosis




Effects of DHT on Various Other Biological Processes and Tissues
*Erythropoiesis
*Lipids
*Skin

*Body composition

-Impact of exogenous DHT therapy on body composition
-Effects of 5a-reductase inhibition therapy and BMD on body composition

*Metabolic syndrome and type 2 diabetes
*Sexual function
*5a-reductase deficiency
*Gynecomastia
*Cognition
*Telomere length




In summary, we have reviewed the evidence that slightly to moderately elevated DHT concentrations or an elevated DHT/T ratio during androgen therapy (most notably, TRT) are unlikely to pose either a higher risk or a unique risk compared with T. We acknowledge that the available published data are limited by the lack of large, well-controlled studies of the long duration that are sufficiently powered to expose subtle safety signals. Nonetheless, the preponderance of available clinical data leads to the conclusion that modest elevations in circulating levels of DHT in response to androgen therapy should not be of concern in clinical practice.

Here are some links that provide strong evidence in DHT's role in cardiovascular disease.






 

madman

Member
Here are some links that provide strong evidence in DHT's role in cardiovascular disease.







The paper I posted is recent!
 

madman

Member
Whats happening to me is even more recent!
*This is just a warning to anyone who is on AI's or is trying to raise his DHT. If you can, please get off it before your heart stops tolerating androgens. Google DHT and heart and you will find links. Testosterones beneficial effects on heart are caused by its conversion to Estrogen while its deleterious effects are caused by its conversion toDHT. Of course this will not be true for everyone but there is a good chance you will screw your heart like me. Look it up.


Sounds frantic to me and to go on claiming that.....Testosterones beneficial effects on the heart are caused by its conversion to Estrogen while its deleterious effects are caused by its conversion to DHT.....is very misleading!

Post up your labs (TT, FT, estradiol, DHT, CBC) for the various protocols you have been on.

Where did your RBCs/hemoglobin/hematocrit sit on such protocol?

Keep in mind that testosterone--->DHT has a tonic effect on the CNS which can make one feel amped up.
 

Michael D

New Member
I'm not an MD, but I am an active researcher with a Ph.D. From my perspective you have too many variables in play to have confidence in what's really going on with your endocrine system. You've been taking a lot of supplements. It would be better to stop taking everything, do labs, and then add one thing at a time and re-check labs. Have you checked your hematocrit? Too many red blood cells could theoretically cause your heart to thicken since it has to push harder to circulate your blood.
 

Nelson Vergel

Founder, ExcelMale.com

 

Sicillian

New Member
I'm not an MD, but I am an active researcher with a Ph.D. From my perspective you have too many variables in play to have confidence in what's really going on with your endocrine system. You've been taking a lot of supplements. It would be better to stop taking everything, do labs, and then add one thing at a time and re-check labs. Have you checked your hematocrit? Too many red blood cells could theoretically cause your heart to thicken since it has to push harder to circulate your blood.
Whatever I have been taking in the past doesn't matter. It is what is happening for the last 1 and a half years that all clearly points to DHT being the culprit.
Labs are not needed to establish the link in this case because the effects are immediate. They do not happen overtime. If there are multiple substances known to raise a hormone and in hours (most cases) cause problems and there are multiple substances known to block that hormone and bring relief immediately there is a very very good chance that it is that hormone to blame particularly when there are multiple studies implicating it in such problems.

Here is a list of things that now cause immediate heart trouble (chest pain, palpitations, shortness breath, general weakness)

1. Proviron
2. Testosterone (applied to scrotum)
3. DHEA (applied to scrotum)
4. HCG
5. Aromatase Inhibitors.
6. Boron

Here is a list of things that bring relief.

1. Finasteride
2. Rosemary oil/tea (strong anti androgen)
3. Borage oil (contains GLA blocks DHT)
4. Pumpkin seed oil (Blocks DHT)
5. Tibolone (estrogenic compound that shuts down your T)
 
Last edited:

Sicillian

New Member
Sounds frantic to me and to go on claiming that.....Testosterones beneficial effects on the heart are caused by its conversion to Estrogen while its deleterious effects are caused by its conversion to DHT.....is very misleading!
This is not frantic or misleading. It is exactly what the study I posted establishes.

"These observations suggest that DHT is responsible for the detrimental effects on cardiac function/morphology induced by testosterone. This is in agreement with our previous reports showing DHT as an inductor of myocardial damage (Regouat et al., 2018). In contrast, 4-OHA (Ki 3.28 μM) administration (Block et al., 1996) increased MMP-3 (P<0.05) and MMP-13 (P<0.01) expression. These results suggest that testosterone aromatization is associated with cardioprotection"


However, as I said, it may not hold for everyone but a percentage of population.
 

madman

Member
This is not frantic or misleading. It is exactly what the study I posted establishes.

"These observations suggest that DHT is responsible for the detrimental effects on cardiac function/morphology induced by testosterone. This is in agreement with our previous reports showing DHT as an inductor of myocardial damage (Regouat et al., 2018). In contrast, 4-OHA (Ki 3.28 μM) administration (Block et al., 1996) increased MMP-3 (P<0.05) and MMP-13 (P<0.01) expression. These results suggest that testosterone aromatization is associated with cardioprotection"


However, as I said, it may not hold for everyone but a percentage of population.

What that study from 2003 done on rats!

"These observations suggest that DHT is responsible for the detrimental effects on cardiac function/morphology induced by testosterone. This is in agreement with our previous reports showing DHT as an inductor of myocardial damage (Regouat et al., 2018). In contrast, 4-OHA (Ki 3.28 μM) administration (Block et al., 1996) increased MMP-3 (P<0.05) and MMP-13 (P<0.01) expression. These results suggest that testosterone aromatization is associated with cardioprotection"




Notice in post #10 where I stated:

Sounds frantic to me and to go on claiming that.....Testosterones beneficial effects on the heart are caused by its conversion to Estrogen while its deleterious effects are caused by its conversion to DHT.....is very misleading!

I specifically underlined while its deleterious effects are caused by its conversion to DHT.

As I and many very well know the important cardioprotective role estradiol plays when it comes to overall health.

If you take the time to search my numerous threads on the forum you will clearly see that I emphasize the importance of having healthy estradiol levels.




Take-home points I have stressed in numerous threads regarding e2!

*Testosterone and more importantly its metabolites estradiol/DHT plays a huge role and are needed in healthy amounts to experiencing the full spectrum of beneficial effects.

*As you should very well know having healthy e2 levels are critical due to its beneficial effects on (cardiovascular health, brain health, libido, erectile function, bone health, tendon health, immune system, body composition).
 

madman

Member
Take a step back and think very deeply on this one as Michael D is on point here!

#11
I'm not an MD, but I am an active researcher with a Ph.D. From my perspective, you have too many variables in play to have confidence in what's really going on with your endocrine system. You've been taking a lot of supplements. It would be better to stop taking everything, do labs, and then add one thing at a time and re-check labs. Have you checked your hematocrit? Too many red blood cells could theoretically cause your heart to thicken since it has to push harder to circulate your blood.
 

TorontoTRT

Active Member
Your problem was “low dose” TE. 70 mg a week is not enough to keep your levels even normal. Studies clearly show this.
 

JA Battle

Active Member
Your problem was “low dose” TE. 70 mg a week is not enough to keep your levels even normal. Studies clearly show this.

Not to start a huge debate but this is not true. I’m on 59.5mg of combined test e/test p weekly split into 5.5mg/3mg daily. My daily numbers are roughly 680 in morning then 3 hours after inject 1000. Shbg is 35. Not only are these numbers normal they are optimal.
 

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