Just a quick note with some preliminary results, to be updated soon. I wanted to get the word our on Christmas Eve, which the legend says shows how the rest of the year would unfold. So, let's hope 2025 will be a year of truth and that one of the greatest falsehoods in medicine may begin to...
lowtoxinforum.com
IDEALABS STUDY: Estrogen causes prostate cancer (PC), DHT and/or aromatase inhibitor may stop/treat PC
I wonder if estrogen is the cause? Not sure. One thing I find with prostate cancer is most of the people I know who have prostate cancer have 2 things in common, huge guts and jobs that required a lot of sitting…. Maybe that causes the inflammation that triggers the cancer
Poor metabolic health is a major risk factor for prostate cancer, which results in high levels of insulin (one of the most potent growth factors for cancer), inflammation, etc.
TyG index and age are risk factors for prostate cancer, and the interaction between the TyG index and different risk factors may increase the risk of prostate cancer. TyG index has some predictive value for the risk of prostate cancer, and the risk of prostate cancer can be reduced by...
pubmed.ncbi.nlm.nih.gov
TRT is not. Men with active prostate cancer are even being treated with TRT now without any adverse effects on progression or mortality:
In this population-based study, testosterone therapy for men on active surveillance for prostate cancer did not worsen mortality. Keywords: Testosterone, Prostate cancer, Outcomes, Active surveillance
pmc.ncbi.nlm.nih.gov
Look into the saturation model of androgens in the prostate. It takes a very low level of serum testosterone (like serious hypogonadism) to produce intraprostate levels of DHT that fully saturate the AR receptors. Beyond that point, additional testosterone has no effect. Your older observational studies making correlations between serum free T and prostate cancer risk are countered by far more relevant (to you) modern studies of TRT which show no increased risk of adverse prostate outcomes.
What about the increase in prostate cancer with higher free T?
Also, isn’t dose irrelevant, the labs (ie total T etc) are more of a guide for trt? I did a single shot of 200 mg test cyp and 5 days after inject my total testosterone was 2100!
*Recent literature does not support an increased risk of PCa in hypogonadal men undergoing testosterone therapy. Although it is mandatory to avoid testosterone administration in men with advanced PCa, insufficient long-term prospective data on the safety of testosterone therapy in PCa survivors [144], should prompt caution in choosing to treat symptomatic hypogonadal men in this setting
EAU GUIDELINES ON SEXUAL AND REPRODUCTIVE HEALTH - LIMITED UPDATE APRIL 2024
3.5 Safety and follow-up in hypogonadism management
3.5.4 Prostate cancer (PCa)
A considerable number of observational studies have failed to demonstrate any association between circulating higher testosterone levels and PCa [138]. In contrast, studies investigating the relationship between low levels of testosterone and risk of PCa have found that men with very low levels of fT have a reduced risk of developing low-to-intermediate-grade PCa, but have a non-significantly increased chance of developing high-grade PCa[138]. This peculiar pattern was also reported in trials such as the Health Professionals Follow-up Study, the Prostate Cancer Prevention Trial (PCPT) and the Reduction by Dutasteride of Prostate Cancer Events (REDUCE),with varying magnitudes of significance [139].
A meta-analysis, including 27 placebo-controlled, RCTs, found no evidence of increased PSA levels following testosterone therapy for one-year. When considering eleven studies reporting on the occurrence of PCa, the meta-analysis found no evidence of increased risk of PCa. However, a one year follow-up may be considered too short to draw firm conclusions on the risks of developing PCa. Furthermore, the analysis was restricted to studies with > 1-year follow-up, but no significant changes in PSA levels nor increased risk of PCa were found [132]. After five-year of median follow-up in three independent registry studies with > 1,000 patients undergoing testosterone therapy, PCa occurrence always remained below the reported incidence rate in the general population [140]. Similar results were reported by a large observational study including 10,311 mentreated with testosterone therapy and 28,029 controls with a median follow-up of 5.3 years [141]. The same study, also showed that the risk of PCa was decreased for men in the highest tertile of testosterone therapy cumulative dose exposure as compared with controls [141].
Recently, the TRAVERSE study, a multicenter, randomized, double-blind, placebo-controlled, noninferiority trial involving 5246 men aged 45 to 80 years, who had pre-existing or a high risk of CVD and who have been treated because of low testosterone levels (i.e., total T < 10.4 nmol/L) associated with reported symptoms of hypogonadism, did not show any difference in terms of PCa incidence or high-grade PCa rate between arms (testosterone therapy vs. placebo) at a mean follow-up, was 33.0± (SD) 12.1 months. Conversely, the same trial showed a significantly greater increase from baseline of total PSA in the treatment group as compared with the placebo arm [77].
With regards to PCa survivors, safety in terms of the risk of recurrence and progression has not yet been established. Limited data are available in the literature, with most case series not providing sufficient data to draw definitive conclusions (e.g., insufficient follow-up, small samples, lack of control arms, heterogeneity in study population and treatment regimen, etc.) [142]. A meta-analysis derived from thirteen studies including 608 patients, of whom 109 had a history of high-risk PCa, with follow-up of 1-189.3 months [143], suggested that testosterone therapy did not increase the risk of biochemical recurrence, but the available evidence is poor,limiting data interpretation [143]. Similar considerations can be derived from another, larger meta-analysis of 21 studies [144]. However, it is important to recognise both meta-analyses demonstrated high heterogeneity among the different studies and included a limited number of subjects.An RCT assessing the safety/benefit ratio of testosterone therapy in hypogonadal men successfully treated with prostatectomy for non-aggressive prostate PCa is currently ongoing [145].
In conclusion, recent literature does not support an increased risk of PCa in hypogonadal men undergoing testosterone therapy. Although it is mandatory to avoid testosterone administration in men with advanced PCa, insufficient long-term prospective data on the safety of testosterone therapy in PCa survivors [144], should prompt caution in choosing to treat symptomatic hypogonadal men in this setting. In particular, patients should receive comprehensive counselling regarding the uncertain long-term effects of testosterone therapy in this context, which necessitates further investigation.Due to the lack of strong evidence-based data on safety, the possible use of testosterone therapy in symptomatic hypogonadal men previously treated for PCa should be fully discussed with patients and limited to low-risk individuals.
ABSTRACT Men with hypogonadism have reduced risk of prostate cancer mortality; whether testosterone treatment increases the risk of prostate safety events in men with hypogonadism remains controversial. Several studies including four larger randomized trials — the Testosterone Trials...
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D. CONCLUSIONS
In middle-aged and older men with hypogonadism, who have been carefully screened to exclude those at high risk of prostate cancer or with severe lower urinary tract symptoms, the incidences of high grade or any prostate cancer, acute urinary retention, invasive surgical procedure on the benign prostatic hyperplasia, prostate biopsy, or initiation of new pharmacologic therapy for lower urinary tract symptoms are low. These findings should be viewed in the context of the small number of prostate cancer events in the testosterone studies, the relatively short treatment duration of the trials relative to the long time it may take for carcinogens to induce cancer, and the exclusion of men at high risk for prostate cancer in these trials. A baseline evaluation of prostate cancer risk and implementation of a standardized monitoring plan to minimize the risk of unnecessary prostate biopsies while enabling the detection of high -grade prostate cancers and other prostate safety events, can help optimize the benefit to risk ratio in men receiving TRT. Because PSA screening and monitoring has the potential for harm, the decision to implement PSA monitoring should be made jointly by the patient and the clinician.
What the TRAVERSE Trial did and did not show
At its core, the TRAVERSE Trial shows that TRT of middle-aged and older men with hypogonadism with a PSA <3.0 ng/mL, who had been screened carefully to exclude those at high risk of prostate cancer, is associated with low risk of high grade or any prostate cancer. Several caveats apply to this inference. First,because the numbers and incidence of high grade or any prostate cancer in the two groups were very low, these data should not be interpreted to mean that the incidence was similar in the two groups. Second, even though TRAVERSE is among the longest and the largest trials of TRT, with 14,304 person -23 years of follow-up and an average follow-up duration of 33 months, carcinogens typically take a long period of time to cause cancer. Long-term differences in risk of prostate cancer in men receiving testosterone or placebo are unknown. Third, in line with American Urological Association/Society of Urologic Oncology (AUA/SUO) guidelines, an elevated PSA was repeated in all men prior to consideration of further evaluation (49,50). Additionally, men were provided access to a standardized informational video about the potential benefits and risks of prostate biopsy to ensure shared decision-making regarding their desire for further evaluation. These steps likely reduced the number of persons undergoing prostate biopsy.Fourth, prostate imaging or genetic testing studies were not performed as part of the evaluation; it is possible that the availability of these additional diagnostic studies could have changed the decision to perform prostate biopsy. Finally, men at increased risk of prostate cancer were excluded from the trial; the trial's findings do not apply to men at high risk of prostate cancer.
In this episode, Dr. Morgentaler and Dr. Brandon discuss the controversial topic of testosterone therapy for men diagnosed with or treated for prostate cancer. Chapters 00:00: Introduction to Testosterone and Prostate Cancer - Dr. Morgentaler and Dr. Brandon set the stage by addressing...
https://www.urotoday.com/conference-highlights/aua-2024/aua-2024-prostate-cancer/151946-aua-2024-crossfire-controversies-in-urology-testosterone-therapy-may-be-reasonably-offered-to-men-on-active-surveillance-pro-con.html (UroToday.com) Recent developments in urology have increasingly...
Testosterone Treatment and the Risk of Prostate Adverse Events (2022) Jason A. Levy, DO, MS, Arthur L. Burnett, MD, MBA, Adrian S. Dobs, MD, MHS INTRODUCTION Definition Hypogonadism is a clinical syndrome that results from failure of the testis to produce physiologic concentrations of...
First off anyone who replied should be asking when were labs drawn? (you already answered this)!
It’s test prop, so yea I think 7 am injection it was a good idea to check at 3pm, as I inject daily. And yes I think lowering my free testosterone to normal ranges is healthier, what am I missing here?
As you should know we always want to test at the true trough (lowest point) before your next injection.
You are injecting daily using short-acting esterified T so there is going to be a big difference in peak--->trough.
Unfortunately you tested 8 hrs post-injection and although it gives you a snapshot you clearly missed the peak so your peak TT, FT and estradiol are going to be higher and more importantly you clearly missed the true trough which would be 24 hrs post-injection so your trough TT, FT and estradiol are going to be lower!
You are injecting a sensible dose 11 mg TP daily (77 mg/week) and you are hitting a high-end TT and more importantly high FT 8 hrs post-injection so again your trough FT will be lower so I would not jump the gun here on the need for lowering your dose.
Yes your peak FT will be very high but your trough is not going to be too high!
Secondly how long have you been on the protocol?
Just keep in mind that although steady-state will be reached much quicker on TP than TC/TE you still need to give it a few months before claiming whether it was a success or failure.
You need to retest your TT and more importantly FT and throw estradiol in there too at true trough to see where said protocol (dose of T/injection frequency) has your true trough which would be 24 hrs post-injection in your case!
If you are hitting a descent trough FT which is most likely the case then ride it out for a few months before deciding whether or not you need to tweak the dose otherwise you will end up chasing your tail indefinitely if you jump the gun to soon!
If you have already put in the time and you feel great overall are not experiencing any sides let alone overall blood markers are healthy (mainly RBCs, hemoglobin and hematocrit) then I would stick with it!
Again you are missing critical blood markers RBCs, hemoglobin and hematocrit but there is no point in testing unless you have put in the time.
As I have stated numerous times on the forum over the years where your hematocrit sits 4-6 weeks in is not where it will end up in the long run as again levels will increase within the 1st month of starting therapy or tweaking a protocol by increasing your dose and it will take anywhere from 6-9 months or in some cases up to a year to reach peak levels.
Chances are you may run into issues as your daily peak FT is going to be very high let alone you are still hitting a high FT 8 hrs post-injection and you will most likely still be hitting a descent trough FT.
Poor metabolic health is a major risk factor for prostate cancer, which results in high levels of insulin (one of the most potent growth factors for cancer), inflammation, etc.
TyG index and age are risk factors for prostate cancer, and the interaction between the TyG index and different risk factors may increase the risk of prostate cancer. TyG index has some predictive value for the risk of prostate cancer, and the risk of prostate cancer can be reduced by...
pubmed.ncbi.nlm.nih.gov
TRT is not. Men with active prostate cancer are even being treated with TRT now without any adverse effects on progression or mortality:
In this population-based study, testosterone therapy for men on active surveillance for prostate cancer did not worsen mortality. Keywords: Testosterone, Prostate cancer, Outcomes, Active surveillance
pmc.ncbi.nlm.nih.gov
Look into the saturation model of androgens in the prostate. It takes a very low level of serum testosterone (like serious hypogonadism) to produce intraprostate levels of DHT that fully saturate the AR receptors. Beyond that point, additional testosterone has no effect. Your older observational studies making correlations between serum free T and prostate cancer risk are countered by far more relevant (to you) modern studies of TRT which show no increased risk of adverse prostate outcomes.
Much more to the story here when it comes to T Therapy in men with PCa!
EAU GUIDELINES ON SEXUAL AND REPRODUCTIVE HEALTH - LIMITED UPDATE APRIL 2024
3.5 Safety and follow-up in hypogonadism management
3.5.4 Prostate cancer (PCa)
* In conclusion, recent literature does not support an increased risk of PCa in hypogonadal men undergoing testosterone therapy. Although it is mandatory to avoid testosterone administration in men with advanced PCa, insufficient long-term prospective data on the safety of testosterone therapy in PCa survivors [144], should prompt caution in choosing to treat symptomatic hypogonadal men in this setting. In particular, patients should receive comprehensive counselling regarding the uncertain long-term effects of testosterone therapy in this context, which necessitates further investigation.Due to the lack of strong evidence-based data on safety, the possible use of testosterone therapy in symptomatic hypogonadal men previously treated for PCa should be fully discussed with patients and limited to low-risk individuals.
Testosterone Treatment and the Risk of Prostate Adverse Events (2022) Jason A. Levy, DO, MS, Arthur L. Burnett, MD, MBA, Adrian S. Dobs, MD, MHS INTRODUCTION Definition Hypogonadism is a clinical syndrome that results from failure of the testis to produce physiologic concentrations of...
Poor metabolic health is a major risk factor for prostate cancer, which results in high levels of insulin (one of the most potent growth factors for cancer), inflammation, etc.
TyG index and age are risk factors for prostate cancer, and the interaction between the TyG index and different risk factors may increase the risk of prostate cancer. TyG index has some predictive value for the risk of prostate cancer, and the risk of prostate cancer can be reduced by...
pubmed.ncbi.nlm.nih.gov
TRT is not. Men with active prostate cancer are even being treated with TRT now without any adverse effects on progression or mortality:
In this population-based study, testosterone therapy for men on active surveillance for prostate cancer did not worsen mortality. Keywords: Testosterone, Prostate cancer, Outcomes, Active surveillance
pmc.ncbi.nlm.nih.gov
Look into the saturation model of androgens in the prostate. It takes a very low level of serum testosterone (like serious hypogonadism) to produce intraprostate levels of DHT that fully saturate the AR receptors. Beyond that point, additional testosterone has no effect. Your older observational studies making correlations between serum free T and prostate cancer risk are countered by far more relevant (to you) modern studies of TRT which show no increased risk of adverse prostate outcomes.
you blood work was at peak(ish). prop has high peak/low low. you need to blood work in the morning before injection. there is a reasons most clinics have patients in the 120-180mg range on TRT. again - all individual - so if you do great on a low dose, not dismissing it by any means go for it.
you can also argue that at those low doses TRT does not make a lot of sense, as most people can achieve those levels naturally by modifying diet/lifestyle. chasing any lab is pointless. on the flip side, on such doses you will miss out on many of the TRT benefits, raised DHT (especially with Prop), some anabolism etc. I experimented with many esters, doses and regimens, and function the best at 25-30mg Tprop daily. yes this is outside of what you natural would achieve, but who gives a shit? I have yet to see credible evidence that this is problematic
there is a reasons most clinics have patients in the 120-180mg range on TRT. again -
We can blow holes through this LMFAO!
Still pushing that nonsense!
Most would never even need 180-200 mg T/week in order to achieve a healthy let alone high trough FT.
Throw in the addition of hCG to boot LOL!
F**K most of those T clinics as many are overmedicating men from the get-go!
Again most men on TTh are injecting 100-200 mg T/week whether once weekly or split into more frequent injections as in twice-weekly (every 3.5 days), M/W/F, EOD or daily.
The majority of men can easily hit a healthy let alone high trough FT injecting 100-150 mg T/week especially when split into more frequent injections.
Some men can even achieve stellar levels <100 mg T/week when split into more frequent injections.
Yes there are outliers who may need the high-end therapeutic dose 200 mg T/week but it is far from COMMON as in F**KING RARE!
you can also argue that at those low doses TRT does not make a lot of sense, as most people can achieve those levels naturally by modifying diet/lifestyle. chasing any lab is pointless. on the flip side, on such doses you will miss out on many of the TRT benefits, raised DHT (especially with Prop), some anabolism etc.
Need to tread lightly on that one as again some men can achieve stellar trough/steady-state FT injecting <100 mg T/week when split into more frequent injections.
No chance in hell you could mimic these levels through natty means as your FT levels on injectable esterified T will be elevated 24/7.
Blood levels achieved trough/steady-state on said dose is what truly matters here!
Having healthy FT, estradiol and DHT is all that matters it's a f**king myth that high levels of FT let alone DHT are needed for a healthy libido let alone erectile function!
Pure nonsense pushed by those CLUELESS SHEEP stinking up the so called men's health/HRT forums!
I experimented with many esters, doses and regimens, and function the best at 25-30mg Tprop daily. yes this is outside of what you natural would achieve, but who gives a shit? I have yet to see credible evidence that this is problematic
You sure you really want to go down this road again son?
Give your head a shake!
Again 30 mg TP daily (210 mg/week) is not a therapeutic dose of T!
Go push that nonsense on those bro forums!
30 mg TP daily (210 mg/week) is an absurd weekly dose of T!
Would be the equivalent of banging 249 mg TC/week which is beyond the top-end therapeutic dose of T.
As you should very well know 200 mg T/week is overkill for most!
Feel/function best need to tread lightly on that one too BRUH!
Hello, I tried Kyzatrex at 200mg twice a day for a total of 400mg a day but it only got my total Test to 419. According to their titration guide, I would need 2x200mg twice a day for a total of 800mg a day which becomes cost prohibitive for me. So I have decided to try Test Cypionate instead...
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...
pubmed.ncbi.nlm.nih.gov
pmc.ncbi.nlm.nih.gov
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