Low Ferritin, High Hematocrit. What to do next?

[Anthony52]

Hi Guys,

52 yo male here. I started TRT 4 1/2 months ago due to free test levels of 7.9, range 7.7 to 24. I had every hypogonadism symptom in the book. I have high SHGB and I'm a low estrogen aromatizer. I'd say I'm a TRT hyper responder. I use test enanthate and HCG both injected Mon/Thurs. I really would appreciate need some advice here from the pros.

Labs: (all labs are at trough). All 6 weeks stints include 250IU HCG twice a week. Test Enanthate also injected twice a week)

o 6 weeks at 100mg/wk + 500IU HCG/wk: Total T >1500 | Free T 40.5 - Felt amazing but doctor said too high.
o 6 weeks at 60mg/wk + 500IU HCG/wk: Total T 859 | Free T 15.4 - All TRT benefits vanished. I guess due to high SHBG I need high total T to achieve symptom relieving free T levels.
o 6 weeks at 80mg/wk + 500IU HCG/wk: Total T 1101 | Free T 21.5 – Felt much better vs 60mg/wk at first, but significant fatigue and brain fog crept in over the last 3 weeks. Even with these levels at trough, Estradiol is only 32 so I am a low aromatizer.

I decided to check my Ferritin last week due to the severe fatigue, it was flagged as low 24, range 38 to 380. Pre TRT my Ferritin was 145. I did not check my Ferritin at any other time since starting TRT so I only have Pre TRT levels and most recent levels taken last week.

Hematocrit Pre TRT = 46
Hematocrit during 100mg stint = 47.3
Hematocrit during 60mg stint = 47.5
Hematocrit during 80mg stint = 50.6 (most recent stint)

Interestingly, during the first 12 weeks my Hematocrit only went up a little from Pre TRT levels. But the latest 6 weeks at the 80mg dose shot it way up.

So it's the paradox of not being able to donate blood to bring hematocrit down since it will tank my Ferritin even more, and not being able to aggressively increase my Ferritin with iron pills since it will push my hematocrit even higher.

Option A: Lower dose to 70mg/wk + 500IU HCG/wk + Iron Bisglycinate 25mg M/W/F OR Heme Iron 10.5mg M/W/F until Ferritin comes back up....hopefully without raising HCT too much more???

Option B: Switch to 100mg day of Testosterone Gel (Atrevis Base) on shoulders/upper arms. This option is mainly because I really cannot go any lower than 70mg/wk in order to get a high enough Free T to relieve symptoms due to my high SHGB. However, I'm wondering if lowering to 70mg/week will just prolong the inevitable and my hematocrit will just creep back up again but over a longer period of time and continue draining my Ferritin causing fatigue. So I thought maybe gel/cream is better for my genetic makeup and may cause less hematocrit creep but I have read mixed reviews about if this is actually true? My plan would be once a day morning dosing for gel/cream

What would be the next move if you were me? Option A or B? TRT has been live changing before the low Ferritin fatigue so I'd like to find a way to stay on it but not damage my health with the high hematocrit of the punishing fatigue of the low Ferritin. Thanks very much in advance for the advice!

 

[WhiteMale]

I was never able to treat my subterranean Ferritin, tried everything in the book including using cast iron skillets. No TRT dose changes did anything either. Though I always postulated that if you weren't forcing me to donate every 56 days due to a subjective HCT value there might not be an iron/ferritin problem. I just had this a week ago with a new TRT provider at Defy. I've not run it since I've been on creams and now only have to donate about once per year as my HCT stabilized for the most part. I'll add it to my next labs but I don't think that there's anything to blame in any symptom I have because ferritin is low.

 

[Leeman]

Hi Guys,

52 yo male here. I started TRT 4 1/2 months ago due to free test levels of 7.9, range 7.7 to 24. I had every hypogonadism symptom in the book. I have high SHGB and I'm a low estrogen aromatizer. I'd say I'm a TRT hyper responder. I use test enanthate and HCG both injected Mon/Thurs. I really would appreciate need some advice here from the pros.

Labs: (all labs are at trough). All 6 weeks stints include 250IU HCG twice a week. Test Enanthate also injected twice a week)

o 6 weeks at 100mg/wk + 500IU HCG/wk: Total T >1500 | Free T 40.5 - Felt amazing but doctor said too high.
o 6 weeks at 60mg/wk + 500IU HCG/wk: Total T 859 | Free T 15.4 - All TRT benefits vanished. I guess due to high SHBG I need high total T to achieve symptom relieving free T levels.
o 6 weeks at 80mg/wk + 500IU HCG/wk: Total T 1101 | Free T 21.5 – Felt much better vs 60mg/wk at first, but significant fatigue and brain fog crept in over the last 3 weeks. Even with these levels at trough, Estradiol is only 32 so I am a low aromatizer.

I decided to check my Ferritin last week due to the severe fatigue, it was flagged as low 24, range 38 to 380. Pre TRT my Ferritin was 145. I did not check my Ferritin at any other time since starting TRT so I only have Pre TRT levels and most recent levels taken last week.

Hematocrit Pre TRT = 46
Hematocrit during 100mg stint = 47.3
Hematocrit during 60mg stint = 47.5
Hematocrit during 80mg stint = 50.6 (most recent stint)

Interestingly, during the first 12 weeks my Hematocrit only went up a little from Pre TRT levels. But the latest 6 weeks at the 80mg dose shot it way up.

So it's the paradox of not being able to donate blood to bring hematocrit down since it will tank my Ferritin even more, and not being able to aggressively increase my Ferritin with iron pills since it will push my hematocrit even higher.

Option A: Lower dose to 70mg/wk + 500IU HCG/wk + Iron Bisglycinate 25mg M/W/F OR Heme Iron 10.5mg M/W/F until Ferritin comes back up....hopefully without raising HCT too much more???

Option B: Switch to 100mg day of Testosterone Gel (Atrevis Base) on shoulders/upper arms. This option is mainly because I really cannot go any lower than 70mg/wk in order to get a high enough Free T to relieve symptoms due to my high SHGB. However, I'm wondering if lowering to 70mg/week will just prolong the inevitable and my hematocrit will just creep back up again but over a longer period of time and continue draining my Ferritin causing fatigue. So I thought maybe gel/cream is better for my genetic makeup and may cause less hematocrit creep but I have read mixed reviews about if this is actually true? My plan would be once a day morning dosing for gel/cream

What would be the next move if you were me? Option A or B? TRT has been live changing before the low Ferritin fatigue so I'd like to find a way to stay on it but not damage my health with the high hematocrit of the punishing fatigue of the low Ferritin. Thanks very much in advance for the advice!

I've been there too. First of all, TRT will lower your Ferritin level even without donating. Back when I trusted my clinic and their TRT supervision, I allowed them to completely tank my Iron and Ferritin and the effect was literally as bad as being Hypogonadal. It took me about 6 months (of eating tons of Red Meat, Iron supp's EOD, no tannins and lots of OJ, to name a few) to get it back into any kind of range that began to feel normal again. Then, it was time to DONATE AGAIN!!! -just shoot me

Long boring story short; these idiot Dr's and clinics seldom even monitor Iron and Ferritin and the patient is the one who pays the price. Now, I demand it with EVERY Lab!

FYI; Non anemic Iron deficiency is about TWICE as common as Iron deficient Anemia! I had Non Anemic Iron deficiency and without a specific Iron and Ferritin test, this condition goes undetected...

Dr. Fred Vorck has a good protocol for boosting your Ferritin WITHOUT increasing your Hct and Hb. It's a very good read and I've used it successfully right after a donation when my Ferritin was <15 PRIOR to the donation! and it immediately (7days) got me back to 35 without killing my Hct & Hb.

Fixing High Hemoglobin or Hematocrit and Low Ferritin While on TRT

From what I gather, it's almost impossible to get Ferritin to >75 while on TRT. (50 might even be a stretch) I know it will not happen for me while keeping my Hct & Hb in check with the Bogus BS #'s from Labcorp and Quest. But, while under a Dr's protocol, I have to meet those ridiculous Range #'s. i.e. 50% and 17.5

 

[madman]

Hi Guys,

52 yo male here. I started TRT 4 1/2 months ago due to free test levels of 7.9, range 7.7 to 24. I had every hypogonadism symptom in the book. I have high SHGB and I'm a low estrogen aromatizer. I'd say I'm a TRT hyper responder. I use test enanthate and HCG both injected Mon/Thurs. I really would appreciate need some advice here from the pros.

Labs: (all labs are at trough). All 6 weeks stints include 250IU HCG twice a week. Test Enanthate also injected twice a week)

o 6 weeks at 100mg/wk + 500IU HCG/wk: Total T >1500 | Free T 40.5 - Felt amazing but doctor said too high.
o 6 weeks at 60mg/wk + 500IU HCG/wk: Total T 859 | Free T 15.4 - All TRT benefits vanished. I guess due to high SHBG I need high total T to achieve symptom relieving free T levels.
o 6 weeks at 80mg/wk + 500IU HCG/wk: Total T 1101 | Free T 21.5 – Felt much better vs 60mg/wk at first, but significant fatigue and brain fog crept in over the last 3 weeks. Even with these levels at trough, Estradiol is only 32 so I am a low aromatizer.

I decided to check my Ferritin last week due to the severe fatigue, it was flagged as low 24, range 38 to 380. Pre TRT my Ferritin was 145. I did not check my Ferritin at any other time since starting TRT so I only have Pre TRT levels and most recent levels taken last week.

Hematocrit Pre TRT = 46
Hematocrit during 100mg stint = 47.3
Hematocrit during 60mg stint = 47.5
Hematocrit during 80mg stint = 50.6 (most recent stint)

Interestingly, during the first 12 weeks my Hematocrit only went up a little from Pre TRT levels. But the latest 6 weeks at the 80mg dose shot it way up.

So it's the paradox of not being able to donate blood to bring hematocrit down since it will tank my Ferritin even more, and not being able to aggressively increase my Ferritin with iron pills since it will push my hematocrit even higher.

Option A: Lower dose to 70mg/wk + 500IU HCG/wk + Iron Bisglycinate 25mg M/W/F OR Heme Iron 10.5mg M/W/F until Ferritin comes back up....hopefully without raising HCT too much more???

Option B: Switch to 100mg day of Testosterone Gel (Atrevis Base) on shoulders/upper arms. This option is mainly because I really cannot go any lower than 70mg/wk in order to get a high enough Free T to relieve symptoms due to my high SHGB. However, I'm wondering if lowering to 70mg/week will just prolong the inevitable and my hematocrit will just creep back up again but over a longer period of time and continue draining my Ferritin causing fatigue. So I thought maybe gel/cream is better for my genetic makeup and may cause less hematocrit creep but I have read mixed reviews about if this is actually true? My plan would be once a day morning dosing for gel/cream

What would be the next move if you were me? Option A or B? TRT has been live changing before the low Ferritin fatigue so I'd like to find a way to stay on it but not damage my health with the high hematocrit of the punishing fatigue of the low Ferritin. Thanks very much in advance for the advice!

You just dove in head first here, this is a complete mess!

You are only 4.5 months in and already tweaked your dose of T three times!

When it comes to where you hematocrits sits means jack s**t 6 weeks in and if you were only doing 6 weeks stints then tweaking your dose you would need to go back to square one as in giving said protocol (dose of T/injection frequency) 3-6 months to see where your hematocrit would have truly ended up.

When first starting T therapy or tweaking a protocol (increasing dose of T) hematocrit will start to rise within the first month and the s**t kicker here is the biggest increase will be seen at the 3-6 month mark then levels will tend to stabilize for most but even then some men can still see an increase up to 9-12 months before levels fully stabilize.

Where your hematocrit sits on said protocol 1 month in let alone 3 months in is not where it will end up.

What is even more concerning here is you lack the understanding of how exogenous T works seeing as you kept switching up your protocol every 6 weeks.


Labs: (all labs are at trough). All 6 weeks stints include 250IU HCG twice a week. Test Enanthate also injected twice a week)

o 6 weeks at 100mg/wk + 500IU HCG/wk: Total T >1500 | Free T 40.5 - Felt amazing but doctor said too high.
o 6 weeks at 60mg/wk + 500IU HCG/wk: Total T 859 | Free T 15.4 - All TRT benefits vanished. I guess due to high SHBG I need high total T to achieve symptom relieving free T levels.
o 6 weeks at 80mg/wk + 500IU HCG/wk: Total T 1101 | Free T 21.5 – Felt much better vs 60mg/wk at first, but significant fatigue and brain fog crept in over the last 3 weeks.

Interestingly, during the first 12 weeks my Hematocrit only went up a little from Pre TRT levels. But the latest 6 weeks at the 80mg dose shot it way up.
I decided to check my Ferritin last week due to the severe fatigue, it was flagged as low 24, range 38 to 380. Pre TRT my Ferritin was 145. I did not check my Ferritin at any other time since starting TRT so I only have Pre TRT levels and most recent levels taken last week.

Hematocrit Pre TRT = 46
Hematocrit during 100mg stint = 47.3
Hematocrit during 60mg stint = 47.5
Hematocrit during 80mg stint = 50.6 (most recent stint)

Interestingly, during the first 12 weeks my Hematocrit only went up a little from Pre TRT levels. But the latest 6 weeks at the 80mg dose shot it way up.


The first 6 weeks means nothing when looking at the bigger picture here!

You are going to be left chasing your tail endlessly if you keep increasing/decresing your dose every 6 weeks.

This is a given!

You need to give a protocol 12 weeks to truly gauge the outcome here.

Keep in mind when first starting TTh or tweaking a protocol the weeks leading up until blood levels have stabilized mean nothing when looking at the bigger picture here as your hormones will be in flux during the weeks leading up until steady-state is achieved and it is common for one to experience ups/downs along the way as the body is trying to adjust to the increase in T and its metabolites (estradiol/DHT).

Many tend to experience what is called the honeymoon period where one feels euphoric, increased libido and erections and overall well-being due to increased dopamine, rising T and lighting up of the ARs (androgen receptors).

Unfortunately this is short-lived and temporary as the body will eventually adapt and things tend to wane back in the norm as in healthy.

Even then once steady-state is achieved it will still take the body time as in a few more months to adapt to its new set-point and this is the critical time period where one needs to gauge how they truly feel overall regarding relief/improvement of low-T symptoms and overall well-being.

When using TE or TC it will take 4-6 weeks to reach steady-state so the first 4-6 weeks means nothing when looking at the bigger picture here as the body is trying to ADJUST to the rising T.

Once steady-state is achieved it will take a few more months for the body to ADAPT to its new set-point.

Every protocol needs to be given a fighting chance at least 12 weeks before claiming whether it was a success or failure.

Even then I would not put to much weight behind your lab results for free testosterone seeing as chances are you never had it tested using the most accurate assay.

Unfortunately many clueless doctors and patients doing their own labs are still caught up using the known to be inaccurate direct immunoassay (RIA/CLIA) which no one should be using/relying on when it comes to testing the most critical fraction FREE TESTOSTERONE!

52 yo male here. I started TRT 4 1/2 months ago due to free test levels of 7.9, range 7.7 to 24.

Seeing as you had your baseline FT most likely tested using the direct IA based on the reference range which is very similar to Labcorps direct IA then you most likely had your FT tested on all three different protocols using the same known to be inaccurate assay.

Are you sure it was not 7.2-24?

144980: Testosterone, Free, Direct

Labcorp test details for Testosterone, Free, Direct

www.labcorp.com

The only way to know where your FT truly sits would be testing it using the most accurate assay the gold standard Equilibrium Dialysis especially in cases of altered SHBG.

Otherwise you would need to use/rely on the next best testing method the calculated linear law-of-mass action Vermeulen (cFTV) which will give a good approximation.

Plug in your TT, SHBG and Albumin to see where your FT sits!

Free & Bioavailable Testosterone calculator

Just so you have a better understanding of ferritin and T therapy!

post #43/47/51/54/62

V

Thread 'Sleeping much better on Kyzatrex vs injections'

Apr 21, 2026

I had been on daily subq injections of T cyp for 7 years. During the entire time, my sleep quality was pretty poor. It would take 30-60 minutes for me to fall asleep. I would wake 1-3 times each night to go to the bathroom (1 was a good night, 3 a bad night). I would average a good 3-4 hour block of sleep plus 1-3 hours of fragmented sleep each night. On a bad night, I'd get 3+1 hours of sleep. On a great night, I'd get 4+3 hours of sleep. On average I would get 3+2.5 hours of sleep.

I tried melatonin, magnesium, glycinate and some other supplements that seemed to have no effect. I tried...

• Vman
• cypionate injections kyzatrex Oral T sleep sleep quality sleep supplements subcutaneous injections subq subq injections testosterone
• Replies: 64
• Forum: Testosterone Basics & Questions

• 

Thread 'High Hematocrit on TRT: practical “numbers plus action” guide'

Feb 24, 2026

How often should men on TRT check their hematocrit?​

The standard monitoring schedule includes a baseline CBC before starting TRT, a recheck at 3 to 6 weeks, another at 3 months, and then at 6 and 12 months once stable. Any dose or formulation change resets the monitoring clock, requiring a recheck 4 to 6 weeks later. Men with risk factors for elevated hematocrit (sleep apnea, smoking, COPD, or a history of clotting) should check more frequently: every 3 months until the trend is stable.




* The monitoring schedule, the intervention ladder, and the attention...

• madman
• hypogonadism; t-therapy; hematocrit; cvd
• Replies: 6
• Forum: Testosterone Side Effect Management

 

[madman]

Hi Guys,

52 yo male here. I started TRT 4 1/2 months ago due to free test levels of 7.9, range 7.7 to 24. I had every hypogonadism symptom in the book. I have high SHGB and I'm a low estrogen aromatizer. I'd say I'm a TRT hyper responder. I use test enanthate and HCG both injected Mon/Thurs. I really would appreciate need some advice here from the pros.

Labs: (all labs are at trough). All 6 weeks stints include 250IU HCG twice a week. Test Enanthate also injected twice a week)

o 6 weeks at 100mg/wk + 500IU HCG/wk: Total T >1500 | Free T 40.5 - Felt amazing but doctor said too high.
o 6 weeks at 60mg/wk + 500IU HCG/wk: Total T 859 | Free T 15.4 - All TRT benefits vanished. I guess due to high SHBG I need high total T to achieve symptom relieving free T levels.
o 6 weeks at 80mg/wk + 500IU HCG/wk: Total T 1101 | Free T 21.5 – Felt much better vs 60mg/wk at first, but significant fatigue and brain fog crept in over the last 3 weeks. Even with these levels at trough, Estradiol is only 32 so I am a low aromatizer.

I decided to check my Ferritin last week due to the severe fatigue, it was flagged as low 24, range 38 to 380. Pre TRT my Ferritin was 145. I did not check my Ferritin at any other time since starting TRT so I only have Pre TRT levels and most recent levels taken last week.

Hematocrit Pre TRT = 46
Hematocrit during 100mg stint = 47.3
Hematocrit during 60mg stint = 47.5
Hematocrit during 80mg stint = 50.6 (most recent stint)

Interestingly, during the first 12 weeks my Hematocrit only went up a little from Pre TRT levels. But the latest 6 weeks at the 80mg dose shot it way up.

So it's the paradox of not being able to donate blood to bring hematocrit down since it will tank my Ferritin even more, and not being able to aggressively increase my Ferritin with iron pills since it will push my hematocrit even higher.

Option A: Lower dose to 70mg/wk + 500IU HCG/wk + Iron Bisglycinate 25mg M/W/F OR Heme Iron 10.5mg M/W/F until Ferritin comes back up....hopefully without raising HCT too much more???

Option B: Switch to 100mg day of Testosterone Gel (Atrevis Base) on shoulders/upper arms. This option is mainly because I really cannot go any lower than 70mg/wk in order to get a high enough Free T to relieve symptoms due to my high SHGB. However, I'm wondering if lowering to 70mg/week will just prolong the inevitable and my hematocrit will just creep back up again but over a longer period of time and continue draining my Ferritin causing fatigue. So I thought maybe gel/cream is better for my genetic makeup and may cause less hematocrit creep but I have read mixed reviews about if this is actually true? My plan would be once a day morning dosing for gel/cream

What would be the next move if you were me? Option A or B? TRT has been live changing before the low Ferritin fatigue so I'd like to find a way to stay on it but not damage my health with the high hematocrit of the punishing fatigue of the low Ferritin. Thanks very much in advance for the advice!

You should have thought this through before jumping on T.

Unfortunately you have already wasted the first 4.5 months chasing your tail here.


* Following the initiation of testosterone therapy, serum concentrations of testosterone are known to correct earlier than the symptomatic, structural, and metabolic signs associated with TD.76,77








26.What is a reasonable timeline to begin to observe improvements in the signs and symptoms of testosterone deficiency?

* Following the initiation of testosterone therapy, serum concentrations of testosterone are known to correct earlier than the symptomatic, structural, and metabolic signs associated with TD.76,77 As such, patients should be counseled that symptom response will not be immediate. Expectations for treatment response should be established with each patient. Patients can anticipate improvements in many of the common symptoms of TD (libido, energy levels, sexual function) after 3 months of treatment or longer. Metabolic and structural (body composition, muscle mass, bone density) changes may take upwards of 6-months. 77 In addition, patients should be counseled that diet and exercise in combination with testosterone therapy are recommended for body composition changes.


* Appreciating this pattern of response to testosterone therapy is fundamental when determining the impact of treatment and the appropriate timing of follow-up evaluations while on therapy. For example, if patients undergo a symptom review and measurement of testosterone levels too early (< 3 months), it may lead both physicians and patients to conclude that the treatment has not been impactful (i.e. normal levels of testosterone without symptomatic/structural/metabolic benefit). However, if the same assessment was scheduled 3-6 months after the initiation of therapy, the clinical response tends to be more reflective of normalized levels of serum testosterone.

Post in thread 'Need Help- New to TRT'

Apr 24, 2026

Overlooked let alone still misunderstood by many!

Newbies. and some of those so called vets littered on the kiddie forums polluting the net!

Years later and we are still doing RERUNS here LMFAO!

Again the first 6 weeks means nothing when looking at the bigger picture here!

I you are not willing to put in the time needed to truly gauge the effectiveness of a protocol as in 12 weeks then you are going to be left chasing your tale endlessly!


*Following the initiation of testosterone therapy, serum concentrations of testosterone are known to correct earlier than the...

• madman

 

[Systemlord]

Eight months ago, I went on TRT and I had donated blood beforehand and realized it was a huge mistake because I felt like shit afterwards. I went onto TRT and felt great for two months before the ferritin caught up with me.

I only respond optimally to TRT with ferritin around 30. I’m not seeing a reason to donate based on your hematocrit numbers. I’ve had my hematocrit as high as 58% and my endocrinologist had been scheduling monthly phlebotomies for a year when a hematologist put a stop to it because my blood pressure numbers (109/53) were better prior to the blood leading session versus after. I was actually experiencing low blood pressure while on a beta blocker during all of this and was forced to stop. Blood pressure still remained normal.

 

[ajallday]

You just dove in head first here, this is a complete mess!

You are only 4.5 months in and already tweaked your dose of T three times!

When it comes to where you hematocrits sits means jack s**t 6 weeks in and if you were only doing 6 weeks stints then tweaking your dose you would need to go back to square one as in giving said protocol (dose of T/injection frequency) 3-6 months to see where your hematocrit would have truly ended up.

When first starting T therapy or tweaking a protocol (increasing dose of T) hematocrit will start to rise within the first month and the s**t kicker here is the biggest increase will be seen at the 3-6 month mark then levels will tend to stabilize for most but even then some men can still see an increase up to 9-12 months before levels fully stabilize.

Where your hematocrit sits on said protocol 1 month in let alone 3 months in is not where it will end up.

What is even more concerning here is you lack the understanding of how exogenous T works seeing as you kept switching up your protocol every 6 weeks.


Labs: (all labs are at trough). All 6 weeks stints include 250IU HCG twice a week. Test Enanthate also injected twice a week)

o 6 weeks at 100mg/wk + 500IU HCG/wk: Total T >1500 | Free T 40.5 - Felt amazing but doctor said too high.
o 6 weeks at 60mg/wk + 500IU HCG/wk: Total T 859 | Free T 15.4 - All TRT benefits vanished. I guess due to high SHBG I need high total T to achieve symptom relieving free T levels.
o 6 weeks at 80mg/wk + 500IU HCG/wk: Total T 1101 | Free T 21.5 – Felt much better vs 60mg/wk at first, but significant fatigue and brain fog crept in over the last 3 weeks.

Interestingly, during the first 12 weeks my Hematocrit only went up a little from Pre TRT levels. But the latest 6 weeks at the 80mg dose shot it way up.
I decided to check my Ferritin last week due to the severe fatigue, it was flagged as low 24, range 38 to 380. Pre TRT my Ferritin was 145. I did not check my Ferritin at any other time since starting TRT so I only have Pre TRT levels and most recent levels taken last week.

Hematocrit Pre TRT = 46
Hematocrit during 100mg stint = 47.3
Hematocrit during 60mg stint = 47.5
Hematocrit during 80mg stint = 50.6 (most recent stint)

Interestingly, during the first 12 weeks my Hematocrit only went up a little from Pre TRT levels. But the latest 6 weeks at the 80mg dose shot it way up.


The first 6 weeks means nothing when looking at the bigger picture here!

You are going to be left chasing your tail endlessly if you keep increasing/decresing your dose every 6 weeks.

This is a given!

You need to give a protocol 12 weeks to truly gauge the outcome here.

Keep in mind when first starting TTh or tweaking a protocol the weeks leading up until blood levels have stabilized mean nothing when looking at the bigger picture here as your hormones will be in flux during the weeks leading up until steady-state is achieved and it is common for one to experience ups/downs along the way as the body is trying to adjust to the increase in T and its metabolites (estradiol/DHT).

Many tend to experience what is called the honeymoon period where one feels euphoric, increased libido and erections and overall well-being due to increased dopamine, rising T and lighting up of the ARs (androgen receptors).

Unfortunately this is short-lived and temporary as the body will eventually adapt and things tend to wane back in the norm as in healthy.

Even then once steady-state is achieved it will still take the body time as in a few more months to adapt to its new set-point and this is the critical time period where one needs to gauge how they truly feel overall regarding relief/improvement of low-T symptoms and overall well-being.

When using TE or TC it will take 4-6 weeks to reach steady-state so the first 4-6 weeks means nothing when looking at the bigger picture here as the body is trying to ADJUST to the rising T.

Once steady-state is achieved it will take a few more months for the body to ADAPT to its new set-point.

Every protocol needs to be given a fighting chance at least 12 weeks before claiming whether it was a success or failure.

Even then I would not put to much weight behind your lab results for free testosterone seeing as chances are you never had it tested using the most accurate assay.

Unfortunately many clueless doctors and patients doing their own labs are still caught up using the known to be inaccurate direct immunoassay (RIA/CLIA) which no one should be using/relying on when it comes to testing the most critical fraction FREE TESTOSTERONE!

52 yo male here. I started TRT 4 1/2 months ago due to free test levels of 7.9, range 7.7 to 24.

Seeing as you had your baseline FT most likely tested using the direct IA based on the reference range which is very similar to Labcorps direct IA then you most likely had your FT tested on all three different protocols using the same known to be inaccurate assay.

Are you sure it was not 7.2-24?

144980: Testosterone, Free, Direct

Labcorp test details for Testosterone, Free, Direct

www.labcorp.com

View attachment 57278


The only way to know where your FT truly sits would be testing it using the most accurate assay the gold standard Equilibrium Dialysis especially in cases of altered SHBG.

Otherwise you would need to use/rely on the next best testing method the calculated linear law-of-mass action Vermeulen (cFTV) which will give a good approximation.

Plug in your TT, SHBG and Albumin to see where your FT sits!

Free & Bioavailable Testosterone calculator

Just so you have a better understanding of ferritin and T therapy!

post #43/47/51/54/62

V

Thread 'Sleeping much better on Kyzatrex vs injections'

Apr 21, 2026

I had been on daily subq injections of T cyp for 7 years. During the entire time, my sleep quality was pretty poor. It would take 30-60 minutes for me to fall asleep. I would wake 1-3 times each night to go to the bathroom (1 was a good night, 3 a bad night). I would average a good 3-4 hour block of sleep plus 1-3 hours of fragmented sleep each night. On a bad night, I'd get 3+1 hours of sleep. On a great night, I'd get 4+3 hours of sleep. On average I would get 3+2.5 hours of sleep.

I tried melatonin, magnesium, glycinate and some other supplements that seemed to have no effect. I tried...

• Vman
• cypionate injections kyzatrex Oral T sleep sleep quality sleep supplements subcutaneous injections subq subq injections testosterone
• Replies: 64
• Forum: Testosterone Basics & Questions

• 

Thread 'High Hematocrit on TRT: practical “numbers plus action” guide'

Feb 24, 2026

How often should men on TRT check their hematocrit?​

The standard monitoring schedule includes a baseline CBC before starting TRT, a recheck at 3 to 6 weeks, another at 3 months, and then at 6 and 12 months once stable. Any dose or formulation change resets the monitoring clock, requiring a recheck 4 to 6 weeks later. Men with risk factors for elevated hematocrit (sleep apnea, smoking, COPD, or a history of clotting) should check more frequently: every 3 months until the trend is stable.




* The monitoring schedule, the intervention ladder, and the attention...

• madman
• hypogonadism; t-therapy; hematocrit; cvd
• Replies: 6
• Forum: Testosterone Side Effect Management

What labcorp code is needed for ED test of free testosterone and LC/MSMS OF total testosterone?

I guess my free t results with 070038 are not accurate?

 

[madman]

What labcorp code is needed for ED test of free testosterone and LC/MSMS OF total testosterone?

I guess my free t results with 070038 are not accurate?

I guess my free t results with 070038 are not accurate?

070038: Testosterone, Free, Equilibrium Ultrafiltration With Total Testosterone, LC/MS-MS

Labcorp test details for Testosterone, Free, Equilibrium Ultrafiltration With Total Testosterone, LC/MS-MS

www.labcorp.com

I and those in the know as in the top experts in the field no longer recommend Equilibrium Ultrafiltratiion as it is more prone to over/underestimating FT.

The gold standard for testing free testosterone is Equilibrium Dialysis.

This is the test number 500726 for the Equilibrium Dialysis assay which also includes the most accurate assay for TT (LC-MS/MS).

500726: Testosterone, Free, Mass Spectrometry/Equilibrium Dialysis (Endocrine Sciences)

Labcorp test details for Testosterone, Free, Mass Spectrometry/Equilibrium Dialysis (Endocrine Sciences)

www.labcorp.com

 

[ajallday]

I guess my free t results with 070038 are not accurate?

070038: Testosterone, Free, Equilibrium Ultrafiltration With Total Testosterone, LC/MS-MS

Labcorp test details for Testosterone, Free, Equilibrium Ultrafiltration With Total Testosterone, LC/MS-MS

www.labcorp.com

I and those in the know as in the top experts in the field no longer recommend Equilibrium Ultrafiltratiion as it is more prone to over/underestimating FT.

The gold standard for testing free testosterone is Equilibrium Dialysis.

This is the test number 500726 for the Equilibrium Dialysis assay which also includes the most accurate assay for TT (LC-MS/MS).

500726: Testosterone, Free, Mass Spectrometry/Equilibrium Dialysis (Endocrine Sciences)

Labcorp test details for Testosterone, Free, Mass Spectrometry/Equilibrium Dialysis (Endocrine Sciences)

www.labcorp.com

Ok, thank you sir.

 

[Leeman]

Eight months ago, I went on TRT and I had donated blood beforehand and realized it was a huge mistake because I felt like shit afterwards. I went onto TRT and felt great for two months before the ferritin caught up with me.

I only respond optimally to TRT with ferritin around 30. I’m not seeing a reason to donate based on your hematocrit numbers. I’ve had my hematocrit as high as 58% and my endocrinologist had been scheduling monthly phlebotomies for a year when a hematologist put a stop to it because my blood pressure numbers (109/53) were better prior to the blood leading session versus after. I was actually experiencing low blood pressure while on a beta blocker during all of this and was forced to stop. Blood pressure still remained normal.

Systemlord, when you say you "went on TRT", I'm assuming a clinical treatment plan? If clinical, did your Endo or Clinic allow you to get to 58%??

How did you conclude your Ferritin values needed to be 30 for TRT to work?

Did you mean 30 and above?

With Hct as high as 58% and donating every month? for a year, I'm wondering if you were on some form of anabolics prior to your TRT plan? Or have you been checked for H63d and C282Y gene and have ruled out any possibility for hereditary Hemochromatosis?

Just trying to understand your situation

Thx

 

[Systemlord]

Systemlord, when you say you "went on TRT", I'm assuming a clinical treatment plan? If clinical, did your Endo or Clinic allow you to get to 58%??

How did you conclude your Ferritin values needed to be 30 for TRT to work?

Did you mean 30 and above?

With Hct as high as 58% and donating every month? for a year, I'm wondering if you were on some form of anabolics prior to your TRT plan? Or have you been checked for H63d and C282Y gene and have ruled out any possibility for hereditary Hemochromatosis?

Just trying to understand your situation

Thx

Yes, a hematologist at the Kaiser infusion center recommended to stop the therapeutic phlebotomies unless I had a specific set of symptoms. My endocrinologist monitors it closely.

I don’t really have my hematocrit that high anymore as I was overdosing on vitamin C, vitamin D and iron supplements which was driving up all my blood parameters.

Took me years to figure out a normal dose of vitamin vitamin C and vitamin D is an overdose for me. 90 mg of vitamin C puts my ferritin from around 30 to 40 all the way up to 400 and the 300 range on TRT.

 

[Leeman]

Yes, a hematologist at the Kaiser infusion center recommended to stop the therapeutic phlebotomies unless I had a specific set of symptoms. My endocrinologist monitors it closely.

I don’t really have my hematocrit that high anymore as I was overdosing on vitamin C, vitamin D and iron supplements which was driving up all my blood parameters.

Took me years to figure out a normal dose of vitamin vitamin C and vitamin D is an overdose for me. 90 mg of vitamin C puts my ferritin from around 30 to 40 all the way up to 400 and the 300 range on TRT.

WOW!! That's wild.

I envy you having a Dr who allowed you to go to 58%. That's prolly a tad higher than I'd be comfortable with. But, I've had 2 Oncologists/Hematologists put in writing that my Clinic should allow me <55% before donation. But, the Clinic is bound to Stone age protocols and refuse to allow me refills above 50%... Truly sucks. It totally F's my Iron and Ferritin #'s and pretty much negates much of the benefits of TRT.

Even the American Urological Assoc. recommends <55% for patients on TRT.

So, while on those supp's, your Ferritin goes to 400, while your Total T is only 300? Crap, for me on TRT my Ferritin never gets above 50 due to unnecessary (mandatory) donations

 

[madman]

WOW!! That's wild.

I envy you having a Dr who allowed you to go to 58%. That's prolly a tad higher than I'd be comfortable with. But, I've had 2 Oncologists/Hematologists put in writing that my Clinic should allow me 55% before donation. But, the Clinic is bound to Stone age protocols and refuse to allow me refills above 50%... Truly sucks. It totally F's my Iron and Ferritin #'s and pretty much negates much of the benefits of TRT.

Even the American Urological Assoc. recommends 55% for patients on TRT.

So, while on those supp's, your Ferritin goes to 400, while your Total T is only 300? Crap, for me on TRT my Ferritin never gets above 50 due to unnecessary (mandatory) donations

His doctor is an idiot and the guy has had numerous issues on T therapy!

Complete mess.

No doctor truly in the know treating a man with exogenous T would sit back and let the patients hematocrit run wild as in above or well above the cutoff 54%.

Action would be taken whether phlebotomy, lowering the dose to bring down the patient's trough/steady-state FT, switching the formulation or in some cases halting therapy temporarily.

Just to clear up any confusion here the 2021 Canadian Urological Association clinical practice guideline on testosterone deficiency set the cutoff for hematocrit ≥ 55%.

* Management strategies for persistent treatment induced polycythemia (hematocrit levels 55% or greater) may include a dose reduction of testosterone (concentration or application frequency), drug holiday, formulation change or blood donation/phlebotomy.

Even then most doctors in the know are still taking action if a patients hematocrit falls 52-54%.

The AUAs cutoff is still 54% and there was no mention of changing this in the 2024 update for specific sections of the 2018 guidelines.

* While on testosterone therapy, a Hct 54% warrants intervention, such as dose reduction or temporary discontinuation.








Canadian Urological Association clinical practice guideline on testosterone deficiency in
men: Evidence-based Q&A (2021)

Monitoring

25.What monitoring is required for a patient receiving testosterone therapy?

After initiating testosterone therapy, patients should have regular monitoring for response to treatment and adverse events. Table 4 summarizes an evidence-based monitoring schedule for patients on testosterone therapy. 5–7,9

Adjustments to treatment dose and delivery can be made based on patient response, adverse events, and bloodwork results. Testosterone levels (+/- gonadotropins) should be measured to determine adherence and absorption of treatment (LE-moderate, strong recommendation).5,6 The recommended timing of testosterone measurement relative to the last treatment dose will vary depending on the testosterone formulation (i.e. mid-cycle for injectables) and patients should be counselled appropriately to ensure accurate interpretation of results and response to treatment.

A patient’s hematocrit should be followed to ensure they are not developing polycythemia. Polycythemia is a common side effect of testosterone therapy and may be associated with thromboembolic events (LE-moderate, strong recommendation).69,74 Management strategies for persistent treatment induced polycythemia (hematocrit levels 55% or greater) may include a dose reduction of testosterone (concentration or application frequency), drug holiday, formulation change or blood donation/phlebotomy.

Prostate specific antigen (PSA) testing and digital rectal examination should be performed to monitor prostate health in accordance with the evidence-based guidelines for prostate cancer screening (LE-low, weak recommendation).75 The Canadian Urological Association guideline on prostate cancer screening and early diagnosis of prostate cancer can serve as a reference in terms of the management of PSA kinetics for men treated with testosterone therapy.75 While discontinuation of testosterone therapy may be advised while investigating a PSA elevation, significant increases in PSA while on testosterone therapy should not be attributed to the use of testosterone alone and should be investigated irrespective of the use or discontinuation testosterone therapy.

Thread 'Canadian Urology Guideline on Testosterone Replacement'

Mar 5, 2021

Canadian Urological Association clinical practice guideline on testosterone deficiency in men: Evidence-based Q&A (2021)
Ethan D. Grober, MD; Yonah Krakowsky, MD; Mohit Khera, MD; Daniel T. Holmes, MD; Jay C. Lee, MD; John E. Grantmyre, MD; Premal Patel, MD; Richard A. Bebb, MD; Ryan Fitzpatrick, MD; Jeffrey D. Campbell, MD; Serge Carrier, MD; Abraham Morgentaler, MD


Introduction

As part of their ongoing commitment to education and best practice standards, the Canadian Urological Association (CUA) solicited the creation of a clinical practice guideline dedicated to...

• madman
• cua clinical practice guideline td in men
• Replies: 12
• Forum: Testosterone and Men's Health Articles

Evaluation and Management of Testosterone Deficiency: AUA Guideline 2018

11. Prior to offering testosterone therapy, clinicians should measure hemoglobin and hematocrit and inform patients regarding the increased risk of polycythemia. (Strong Recommendation; Evidence Level: Grade A)

Prior to commencing testosterone therapy, all patients should undergo a baseline measurement of hemoglobin/hematocrit. If the Hct exceeds 50%, clinicians should consider withholding testosterone therapy until the etiology is formally investigated. While on testosterone therapy, a Hct 54% warrants intervention, such as dose reduction or temporary discontinuation. While the incidence of polycythemia for one particular modality of testosterone compared to another cannot be determined, trials have indicated that injectable testosterone is associated with the greatest treatment-induced increases in hemoglobin/Hct 12.

Thread 'The Evaluation and Management of Testosterone Deficiency AUA Guideline (2018)'

May 5, 2018

Evaluation and Management of Testosterone Deficiency: AUA Guideline (2018)

John P. Mulhall, Landon W. Trost, Robert E. Brannigan, Emily G. Kurtz, J. Bruce Redmon, Kelly A. Chiles, Deborah J. Lightner, Martin M. Miner, M. Hassan Murad, Christian J. Nelson, Elizabeth A. Platz, Lakshmi V. Ramanathan and Ronald W. Lewis

​

​

Understanding the Impact of Testosterone Therapy on Various Health Conditions​

Testosterone therapy is a common treatment used to address various medical conditions, but its effects are complex and can vary depending on multiple factors. Here's a...

• madman
• Replies: 2
• Forum: Testosterone and Men's Health Articles

Thread 'Update to the Testosterone Deficiency: AUA Guideline 2018'

Mar 8, 2024

CV DISEASE

Results overall provide more definitive evidence that testosterone therapy (when performed appropriately) does not increase the risk for major CV events after a mean 2 years of treatment. The secondary findings of increased arrhythmias, atrial fibrillation, and minimally elevated blood pressure may be due to a volume-expanding effect of testosterone and are of limited/unclear clinical relevance. It is also plausible that the CV risk profile of testosterone may differ depending on doses and agent/modality prescribed (ie, injectable vs topical)...

• madman
• testosterone; cvd/pca/diabetes/osa/sexual function
• Replies: 2
• Forum: Testosterone and Men's Health Articles

Hematocrit thresholds and indications for intervention

• The Endocrine Society:
  • Hematocrit threshold of > 50% is relative contraindication to initiating testosterone therapy.
  • Testosterone therapy can cause erythrocytosis (hematocrit > 54%).
  • Hematocrit threshold of >54% is an indication to discontinue treatment.
  • Clinicians should evaluate men who develop erythrocytosis during testosterone-replacement therapy and withhold testosterone therapy until hematocrit has returned to the normal range and then resume testosterone therapy at a lower dose.
  • Using therapeutic phlebotomy to lower hematocrit is also effective in managing testosterone treatment–induced erythrocytosis.

• The European Association of Urology (EAU):
  • The clinical significance of a high hematocrit level is unclear, but it may be associated with hyperviscosity and thrombosis.
  • If testosterone is prescribed then testosterone levels should not exceed the mid-normal range and the hematocrit should not exceed 54%.
  • Monitor testosterone, hematocrit at three, six and twelve months and thereafter annually.
    • Decrease the testosterone dosage or switch testosterone preparation from intramuscular to topical or venesection.
    • If hematocrit remains elevated, stop testosterone and reintroduce at a lower dose once hematocrit has normalized.
    • Venesection (500 mL) may be considered and repeated if necessary.
  • The hematocrit value of > 54% is based on the increased risk of cardiovascular mortality from the Framingham Heart Study.

• ISA, ISSAM, EAU, EAA and ASA:
  • Men with significant erythrocytosis (hematocrit >52%), untreated obstructive sleep apnea, untreated severe congestive heart failure should not be started on treatment with testosterone without prior resolution of the co-morbid condition.
  • Erythrocytosis can develop during testosterone treatment, especially in older men treated by injectable testosterone preparations. Periodic hematological assessment is indicated, i.e. before treatment, then 3–4 and 12 months in the first year of treatment and annually thereafter.
  • Although it is not yet clear what critical threshold is desirable, dose adjustments and/or periodic phlebotomy may be necessary to keep hematocrit below 52–55%.

• European Academy of Andrology (EAA):
  • We suggest against TRT in men with documented polycythemia and/or elevated hematocrit (>48%-50%) depending on CV risk and associated morbidities without further evaluation.
  • If Hct is >54%, TRT should be discontinued, until Hct decreases to a safe level; evaluate the patient for hypoxia and sleep apnea; reinitiate therapy with a reduced dose.
  • There is a general consensus that Hct > 54% requires TRT withdrawal (and sometimes phlebotomy) to minimize the risks of VTE and CV events.

• American Urological Association (AUA):
  • Prior to offering testosterone therapy, clinicians should measure hemoglobin and hematocrit and inform patients regarding the increased risk of polycythemia.
  • Prior to commencing testosterone therapy, all patients should undergo a baseline measurement of hemoglobin/hematocrit. If the Hct exceeds 50%, clinicians should consider withholding testosterone
    therapy until the etiology is formally investigated.
  • While on testosterone therapy, a Hct 54% warrants intervention, such as:
    • Dose reduction
    • Temporary discontinuation
  • While the incidence of polycythemia for one particular modality of testosterone compared to another cannot be determined, trials have indicated that injectable testosterone is associated with the greatest treatment-induced increases in hemoglobin/Hct.

Note: hematocrit of ≥54% appears to be consistent threshold to discontinuing or reducing treatment utilized by major urologic governing bodies, while the evidence for this specific cutoff is lacking.

Thread 'Testosterone Therapy and Erythrocytosis - the most common dose-limiting effect of testosterone therapy'

Apr 21, 2024

Testosterone Therapy and Erythrocytosis • The Blood Project

Introduction Androgens play a crucial role in the development and maintenance of: Male reproductive and sexual functions Body composition Erythropoiesis

www.thebloodproject.com

Introduction

• Androgens play a crucial role in the development and maintenance of:
  
  • Male reproductive and sexual functions
  • Body composition
  • Erythropoiesis
  • Muscle and bone health
  • Cognitive function
• Testosterone falls progressively with age and a significant percentage of men over the age of 60 years have serum testosterone levels that are below the lower limits of young...

• madman
• hypogonadism; testosterone; hematocrit; cvd
• Replies: 22
• Forum: Testosterone Side Effect Management

• 

 

[Leeman]

His doctor is an idiot and the guy has had numerous issues on T therapy!

Complete mess.

No doctor truly in the know treating a man with exogenous T would sit back and let the patients hematocrit run wild as in above or well above the cutoff 54%.

Action would be taken whether phlebotomy, lowering the dose to bring down the patient's trough/steady-state FT, switching the formulation or in some cases halting therapy temporarily.

Just to clear up any confusion here the 2021 Canadian Urological Association clinical practice guideline on testosterone deficiency set the cutoff for hematocrit ≥ 55%.

* Management strategies for persistent treatment induced polycythemia (hematocrit levels 55% or greater) may include a dose reduction of testosterone (concentration or application frequency), drug holiday, formulation change or blood donation/phlebotomy.

Even then most doctors in the know are still taking action if a patients hematocrit falls 52-54%.

The AUAs cutoff is still 54% and there was no mention of changing this in the 2024 update for specific sections of the 2018 guidelines.

* While on testosterone therapy, a Hct 54% warrants intervention, such as dose reduction or temporary discontinuation.








Canadian Urological Association clinical practice guideline on testosterone deficiency in
men: Evidence-based Q&A (2021)

Monitoring

25.What monitoring is required for a patient receiving testosterone therapy?

After initiating testosterone therapy, patients should have regular monitoring for response to treatment and adverse events. Table 4 summarizes an evidence-based monitoring schedule for patients on testosterone therapy. 5–7,9

Adjustments to treatment dose and delivery can be made based on patient response, adverse events, and bloodwork results. Testosterone levels (+/- gonadotropins) should be measured to determine adherence and absorption of treatment (LE-moderate, strong recommendation).5,6 The recommended timing of testosterone measurement relative to the last treatment dose will vary depending on the testosterone formulation (i.e. mid-cycle for injectables) and patients should be counselled appropriately to ensure accurate interpretation of results and response to treatment.

A patient’s hematocrit should be followed to ensure they are not developing polycythemia. Polycythemia is a common side effect of testosterone therapy and may be associated with thromboembolic events (LE-moderate, strong recommendation).69,74 Management strategies for persistent treatment induced polycythemia (hematocrit levels 55% or greater) may include a dose reduction of testosterone (concentration or application frequency), drug holiday, formulation change or blood donation/phlebotomy.

Prostate specific antigen (PSA) testing and digital rectal examination should be performed to monitor prostate health in accordance with the evidence-based guidelines for prostate cancer screening (LE-low, weak recommendation).75 The Canadian Urological Association guideline on prostate cancer screening and early diagnosis of prostate cancer can serve as a reference in terms of the management of PSA kinetics for men treated with testosterone therapy.75 While discontinuation of testosterone therapy may be advised while investigating a PSA elevation, significant increases in PSA while on testosterone therapy should not be attributed to the use of testosterone alone and should be investigated irrespective of the use or discontinuation testosterone therapy.

Thread 'Canadian Urology Guideline on Testosterone Replacement'

Mar 5, 2021

Canadian Urological Association clinical practice guideline on testosterone deficiency in men: Evidence-based Q&A (2021)
Ethan D. Grober, MD; Yonah Krakowsky, MD; Mohit Khera, MD; Daniel T. Holmes, MD; Jay C. Lee, MD; John E. Grantmyre, MD; Premal Patel, MD; Richard A. Bebb, MD; Ryan Fitzpatrick, MD; Jeffrey D. Campbell, MD; Serge Carrier, MD; Abraham Morgentaler, MD


Introduction

As part of their ongoing commitment to education and best practice standards, the Canadian Urological Association (CUA) solicited the creation of a clinical practice guideline dedicated to...

• madman
• cua clinical practice guideline td in men
• Replies: 12
• Forum: Testosterone and Men's Health Articles

Evaluation and Management of Testosterone Deficiency: AUA Guideline 2018

11. Prior to offering testosterone therapy, clinicians should measure hemoglobin and hematocrit and inform patients regarding the increased risk of polycythemia. (Strong Recommendation; Evidence Level: Grade A)

Prior to commencing testosterone therapy, all patients should undergo a baseline measurement of hemoglobin/hematocrit. If the Hct exceeds 50%, clinicians should consider withholding testosterone therapy until the etiology is formally investigated. While on testosterone therapy, a Hct 54% warrants intervention, such as dose reduction or temporary discontinuation. While the incidence of polycythemia for one particular modality of testosterone compared to another cannot be determined, trials have indicated that injectable testosterone is associated with the greatest treatment-induced increases in hemoglobin/Hct 12.

Thread 'The Evaluation and Management of Testosterone Deficiency AUA Guideline (2018)'

May 5, 2018

Evaluation and Management of Testosterone Deficiency: AUA Guideline (2018)

John P. Mulhall, Landon W. Trost, Robert E. Brannigan, Emily G. Kurtz, J. Bruce Redmon, Kelly A. Chiles, Deborah J. Lightner, Martin M. Miner, M. Hassan Murad, Christian J. Nelson, Elizabeth A. Platz, Lakshmi V. Ramanathan and Ronald W. Lewis

​

​

Understanding the Impact of Testosterone Therapy on Various Health Conditions​

Testosterone therapy is a common treatment used to address various medical conditions, but its effects are complex and can vary depending on multiple factors. Here's a...

• madman
• Replies: 2
• Forum: Testosterone and Men's Health Articles

Thread 'Update to the Testosterone Deficiency: AUA Guideline 2018'

Mar 8, 2024

CV DISEASE

Results overall provide more definitive evidence that testosterone therapy (when performed appropriately) does not increase the risk for major CV events after a mean 2 years of treatment. The secondary findings of increased arrhythmias, atrial fibrillation, and minimally elevated blood pressure may be due to a volume-expanding effect of testosterone and are of limited/unclear clinical relevance. It is also plausible that the CV risk profile of testosterone may differ depending on doses and agent/modality prescribed (ie, injectable vs topical)...

• madman
• testosterone; cvd/pca/diabetes/osa/sexual function
• Replies: 2
• Forum: Testosterone and Men's Health Articles

Hematocrit thresholds and indications for intervention

• The Endocrine Society:
  • Hematocrit threshold of > 50% is relative contraindication to initiating testosterone therapy.
  • Testosterone therapy can cause erythrocytosis (hematocrit > 54%).
  • Hematocrit threshold of >54% is an indication to discontinue treatment.
  • Clinicians should evaluate men who develop erythrocytosis during testosterone-replacement therapy and withhold testosterone therapy until hematocrit has returned to the normal range and then resume testosterone therapy at a lower dose.
  • Using therapeutic phlebotomy to lower hematocrit is also effective in managing testosterone treatment–induced erythrocytosis.

• The European Association of Urology (EAU):
  • The clinical significance of a high hematocrit level is unclear, but it may be associated with hyperviscosity and thrombosis.
  • If testosterone is prescribed then testosterone levels should not exceed the mid-normal range and the hematocrit should not exceed 54%.
  • Monitor testosterone, hematocrit at three, six and twelve months and thereafter annually.
    • Decrease the testosterone dosage or switch testosterone preparation from intramuscular to topical or venesection.
    • If hematocrit remains elevated, stop testosterone and reintroduce at a lower dose once hematocrit has normalized.
    • Venesection (500 mL) may be considered and repeated if necessary.
  • The hematocrit value of > 54% is based on the increased risk of cardiovascular mortality from the Framingham Heart Study.

• ISA, ISSAM, EAU, EAA and ASA:
  • Men with significant erythrocytosis (hematocrit >52%), untreated obstructive sleep apnea, untreated severe congestive heart failure should not be started on treatment with testosterone without prior resolution of the co-morbid condition.
  • Erythrocytosis can develop during testosterone treatment, especially in older men treated by injectable testosterone preparations. Periodic hematological assessment is indicated, i.e. before treatment, then 3–4 and 12 months in the first year of treatment and annually thereafter.
  • Although it is not yet clear what critical threshold is desirable, dose adjustments and/or periodic phlebotomy may be necessary to keep hematocrit below 52–55%.

• European Academy of Andrology (EAA):
  • We suggest against TRT in men with documented polycythemia and/or elevated hematocrit (>48%-50%) depending on CV risk and associated morbidities without further evaluation.
  • If Hct is >54%, TRT should be discontinued, until Hct decreases to a safe level; evaluate the patient for hypoxia and sleep apnea; reinitiate therapy with a reduced dose.
  • There is a general consensus that Hct > 54% requires TRT withdrawal (and sometimes phlebotomy) to minimize the risks of VTE and CV events.

• American Urological Association (AUA):
  • Prior to offering testosterone therapy, clinicians should measure hemoglobin and hematocrit and inform patients regarding the increased risk of polycythemia.
  • Prior to commencing testosterone therapy, all patients should undergo a baseline measurement of hemoglobin/hematocrit. If the Hct exceeds 50%, clinicians should consider withholding testosterone
    therapy until the etiology is formally investigated.
  • While on testosterone therapy, a Hct 54% warrants intervention, such as:
    • Dose reduction
    • Temporary discontinuation
  • While the incidence of polycythemia for one particular modality of testosterone compared to another cannot be determined, trials have indicated that injectable testosterone is associated with the greatest treatment-induced increases in hemoglobin/Hct.

Note: hematocrit of ≥54% appears to be consistent threshold to discontinuing or reducing treatment utilized by major urologic governing bodies, while the evidence for this specific cutoff is lacking.

Thread 'Testosterone Therapy and Erythrocytosis - the most common dose-limiting effect of testosterone therapy'

Apr 21, 2024

Testosterone Therapy and Erythrocytosis • The Blood Project

Introduction Androgens play a crucial role in the development and maintenance of: Male reproductive and sexual functions Body composition Erythropoiesis

www.thebloodproject.com

Introduction

• Androgens play a crucial role in the development and maintenance of:
  
  • Male reproductive and sexual functions
  • Body composition
  • Erythropoiesis
  • Muscle and bone health
  • Cognitive function
• Testosterone falls progressively with age and a significant percentage of men over the age of 60 years have serum testosterone levels that are below the lower limits of young...

• madman
• hypogonadism; testosterone; hematocrit; cvd
• Replies: 22
• Forum: Testosterone Side Effect Management

• 

Agreed. I should have written <55%. Which in my mind meant 54%. I'll update (correct) my future comments to read 54%.

I never had any Hct or Hb issues prior to TRT. (but, that was 10yrs+ ago) But, I Powerlift, don't do much in the way of specific cardio, (I get plenty of moderate to high Heart rate as well as Z1-2 cardio in my training) I have a larger neck, very slight sleep apnea, (did a sleep test) and nasal/sinus restriction that forces me to mouth breath most of my day/night.

So, given everything I've learned, hypoxia is a main driver of high Hb and Hct and TRT is secondary. The two combined are about like living at Attitude and I am fine with the data on people living at altitude and typically Not routinely being forced to be Phlebotomized.

I believe this cond is properly classified as; "secondary erythrocytosis" (as opposed to Polycythemia) I do not believe secondary erythrocytosis carries the same risk and the same denotation as Polycythemia and certainly not PV.

Madman, what's your thoughts on TRT and secondary erythrocytosis Vs. secondary Polycythemia? Am I missing something?

 

[madman]

Agreed. I should have written <55%. Which in my mind meant 54%. I'll update (correct) my future comments to read 54%.

I never had any Hct or Hb issues prior to TRT. (but, that was 10yrs+ ago) But, I Powerlift, don't do much in the way of specific cardio, (I get plenty of moderate to high Heart rate as well as Z1-2 cardio in my training) I have a larger neck, very slight sleep apnea, (did a sleep test) and nasal/sinus restriction that forces me to mouth breath most of my day/night.

So, given everything I've learned, hypoxia is a main driver of high Hb and Hct and TRT is secondary. The two combined are about like living at Attitude and I am fine with the data on people living at altitude and typically Not routinely being forced to be Phlebotomized.

I believe this cond is properly classified as; "secondary erythrocytosis" (as opposed to Polycythemia) I do not believe secondary erythrocytosis carries the same risk and the same denotation as Polycythemia and certainly not PV.

Madman, what's your thoughts on TRT and secondary erythrocytosis Vs. secondary Polycythemia? Am I missing something?

I've had 2 Oncologists/Hematologists put in writing that my Clinic should allow me 55% before donation. But, the Clinic is bound to Stone age protocols and refuse to allow me refills above 50%... Truly sucks. It totally F's my Iron and Ferritin #'s and pretty much negates much of the benefits of TRT.


Your provider clearly has no experience at this when it comes to those outdated stone-aged protocols or addressing elevated hematocrit if it creeps above 50%.

Find a new provider and get off that donating merry go round.




So, given everything I've learned, hypoxia is a main driver of high Hb and Hct and TRT is secondary.


Testosterone itself is a potent dose-dependent stimulus for erythropoiesis.

Many men who develop elevated Hct on T therapy do not have a significant hypoxic driver and even when factors such as OSA, obesity, smoking, or altitude are present maintaining chronically high FT levels especially high trough/steady-state FT provides a substantial erythropoietic stimulus.

I think T therapy and hypoxia are best viewed as additive factors but keep in mind when free T is maintained well above physiologic levels the androgen exposure itself can be the major driver of hematocrit elevation in many men.

Underlying hypoxic conditions can further amplify the response and are especially relevant in those who develop more significant elevations.

As I have stated numerous times on the forum it's not just the supraphysiologic peaks that have an impact on driving up the hematocrit as running too high a trough/steady-state FT will have a huge impact on pushing up the hematocrit.

Unfortunately too many men especially the ones caught up on that more T is better mentality bulls**t being pushed by all those sheep stinking up those so called mens health/HRT forums are running a very high trough FT as in levels that are elevated 24/7 steady-state.

The body was never meant to be amped up on T day in and day out 24/7.

Even if you move to more frequent injections as in dailies to clip the peak--->trough (minimal) and to maintain more stable blood levels throughout the week one can easily still struggle with elevated. hematocrit if they are still running too high a steady-state FT level.

In a patient without significant underlying risk factors such as untreated OSA, chronic hypoxia, smoking, uncontrolled hypertension, or CVD who is otherwise tolerating T therapy well many experienced clinicians would not automatically panic over a stable hematocrit around 50–54%.

They would assess the entire clinical picture including symptoms, trends, TT/FT levels, dosing, BP and potential contributors rather than treating the hematocrit value in isolation.



* No evidence of increased risk when elevated hematocrit is due to TTh

* Erythrocytosis suggests a possible cause of VTE and CV events with TTh, however no evidence of any association

* The hematocrit level at which the risk of neuro-occlusive events or cardiovascular events increases is not known

* Implication - 54% is an arbitrary cut-off

* The frequency of neuro-occlusive events in men with hypogonadism enrolled in RCTs of T who developed erythrocytosis has been very low

* Implications - little evidence of actual vascular risks associated with elevated hematocrit




What's that Abe?

* 54% is a useful, reasonable upper limit of acceptability


Come again, say it ain't so Abe!

* NO NEED TO INTERVENE unless HCT >54%

Thread 'Testosterone Therapy and erythrocytosis'

Jun 20, 2023

Testosterone Therapy and Men’s Health – Demystifying the Hype with Science to Provide Cutting-Edge Treatment for Your Patients (2021)

Summary 25:10-43:34 (Endocrine Society 2018 Guidelines)

Other Risks with Testosterone Therapy and How to Manage Them - T4L Education

t4leducation.com

• madman
• trt; erythrocytosis; hematocrit
• Replies: 7
• Forum: Testosterone Side Effect Management

• 

Sit back and dwell on this one!

*There is no evidence that an increase of haematocrit up to and including 54% causes any adverse effects. If the haematocrit exceeds 54% there is a testosterone independent, but weak associated rise in CV events and mortality [79, 177-179]. Any relationship is complex as these studies were based on patients with any cause of secondary polycythaemia, which included smoking and respiratory diseases. There have been no specific studies in men with only testosterone-induced erythrocytosis

Thread 'Transformative Insights from the Landmark Traverse Trial: A new era in testosterone therapy'

Apr 26, 2024

Nelson's house is where it's at!

• madman
• traverse; testosterone therapy; pca/cvd
• Replies: 22
• Forum: Testosterone and Men's Health Articles

• 

Some key takeaways here:

Cardiovascular Disease (CVD)

*Current available data from interventional studies suggest that there is no increased risk up to three years of testosterone therapy [167-171]. The currently published evidence has reported that testosterone therapy in men with diagnosed hypogonadism has neutral or beneficial actions on MACE in patients with normalised testosterone levels. The findings could be considered sufficiently reliable for at least a three year course of testosterone therapy, after which no available study can exclude further or long-term CV events [172,173]


Erythrocytosis

*There is no evidence that an increase of haematocrit up to and including 54% causes any adverse effects. If the haematocrit exceeds 54% there is a testosterone independent, but weak associated rise in CV events and mortality [79, 177-179]. Any relationship is complex as these studies were based on patients with any cause of secondary polycythaemia, which included smoking and respiratory diseases. There have been no specific studies in men with only testosterone-induced erythrocytosis.




EAU GUIDELINES ON SEXUAL AND REPRODUCTIVE HEALTH - LIMITED UPDATE APRIL 2024


3.5 Safety and follow-up in hypogonadism management


3.5.5 Cardiovascular Disease

Evidence suggests that hypogonadal men have an increased risk of CVD [146, 147]. Whether or not LOH is a cause or a consequence of atherosclerosis has not been clearly determined. Late-onset hypogonadism is associated with CV risk factors, including central obesity, insulin resistance and hyperglycaemia, dyslipidaemia, pro-thrombotic tendency and chronic inflammatory state [147]. Atherosclerosis is a chronic inflammatory disease, that releases pro-inflammatory cytokines into the circulation, which are known to suppress testosterone release from the HPG axis. Evidence from RCTs of testosterone therapy in men with MetS and/or T2DM demonstrates some benefit in CV risk, including reduced central adiposity, insulin resistance, total cholesterol and LDL-cholesterol and suppression of circulating cytokines [28-30, 35, 147, 148]. However, due to the equivocal nature of these studies, testosterone therapy cannot be recommended for use outside of treatment of specific symptoms.

Published data show that LOH is associated with an increase in all-cause and CVD-related mortality [7, 149-152]. These studies are supported by a meta-analysis that concluded that hypogonadism is a risk factor for cardiovascular morbidity [136] and mortality [153]. Importantly, men with low testosterone when compared to eugonadal men with angiographically proven coronary disease have twice the risk of earlier death [147]. Longitudinal population studies have reported that men with testosterone in the upper quartile of the normal range have a reduced number of CV events compared to men with testosterone in the lower three quartiles[149]. Androgen deprivation therapy for PCa is linked to an increased risk of CVD and sudden death [154].Conversely, two long-term epidemiological studies have reported reduced CV events in men with high normal serum testosterone levels [155, 156]. Erectile dysfunction is independently associated with CVD and may be the first clinical presentation in men with atherosclerosis.

The knowledge that men with hypogonadism and/or ED may have underlying CVD should prompt individual assessment of their CV risk profile. Individual risk factors (e.g., lifestyle, diet, exercise, smoking, hypertension,diabetes and dyslipidaemia) should be assessed and treated in men with pre-existing CVD and in patients receiving androgen deprivation therapy. Cardiovascular risk reduction can be managed by primary care clinicians, but patients should be appropriately counselled by clinicians active in prescribing testosterone therapy [83]. If appropriate, patients should be referred to cardiologists for risk stratification and treatment of comorbidity.

No RCTs have provided a clear answer on whether testosterone therapy affects CV outcomes. The TTrial (n=790) conducted in older men [157], the TIMES2 study (n=220) [29], along with the BLAST studies involving men with Metabolic Syndrome (MetS) and Type 2 Diabetes Mellitus (T2DM), as well as the study involving pre-frail and frail elderly men - all of which lasted for one year, and the T4DM study spanning two years - did not show any increase in Major Adverse Cardiovascular Events (MACE) increase in Major Adverse Cardiovascular Events (MACE) [29,32, 33, 157, 158]. Randomised controlled trials, between three and twelve months, in men with known heart disease treated with testosterone have not found an increase in MACE, but have reported improvement in cardiac ischaemia, angina and functional exercise capacity [159-161]. A large cohort study (n=20,4857 men) found that neither transdermal gel or intramuscular testosterone was associated with an increased risk of composite cardiovascular outcome in men with or without prevalent CVD (mean follow-up 4.3 years) [162]. The European Medicines Agency (EMA) has stated that ‘The Co-ordination Group for Mutual recognition and Decentralisation Procedures-Human (CMDh), a regulatory body representing EU Member States, has agreed by consensus that there is no consistent evidence of an increased risk of heart problems with testosterone in men. However, the product information is to be updated in line with the most current available evidence on safety, and with warnings that the lack of testosterone should be confirmed by signs and symptoms and laboratory tests before treating men with these drugs [163].

Data recently released from the TRAVERSE study confirm the findings of the EMA [77]. The latter is the first double-blind, placebo-controlled, non-inferiority RCT with primary CV safety as an end point. The results showed that testosterone therapy was noninferior to placebo with respect to the incidence of MACE. However, a mild higher incidence of atrial fibrillation, acute kidney injury, and pulmonary embolism was observed in the testosterone group [77]. The latter observations, however, need to be confirmed since previous available data do not support an increased risk of venous thromboembolism [78, 164] or major arrhythmias [165] after testosterone therapy. Similarly, the long-term follow-up (median of 5.1 years since last injection) of the T4DM study showed no differences in self-reported rates of new diagnosis of CVD [166].

In conclusion, current available data from interventional studies suggest that there is no increased risk up to three years of testosterone therapy [167-171]. The currently published evidence has reported that testosterone therapy in men with diagnosed hypogonadism has neutral or beneficial actions on MACE in patients with normalised testosterone levels. The findings could be considered sufficiently reliable for at least a three year course of testosterone therapy, after which no available study can exclude further or long-term CV events [172,173].




3.5.5.1 Cardiac Failure

Testosterone therapy is contraindicated in men with severe chronic cardiac failure because fluid retention may lead to exacerbation of the condition. Some studies have shown that men with moderate chronic cardiac failure may benefit from low doses of testosterone, which achieve mid-normal range testosterone levels [160,174, 175]. An interesting observation is that untreated hypogonadism increased the re-admission and mortality rate in men with heart failure [176]. If a decision is made to treat hypogonadism in men with chronic cardiac failure, it is essential that the patient is followed up carefully with clinical assessment and both testosterone and haematocrit measurements on a regular basis.




3.5.6 Erythrocytosis

An elevated haematocrit level is the most common adverse effect of testosterone therapy. Stimulation of erythropoiesis is a normal biological action that enhances the delivery of oxygen to testosterone-sensitive tissues (e.g., striated, smooth and cardiac muscle). Any elevation above the normal range for haematocrit usually becomes evident between three and twelve months after testosterone therapy initiation. However,polycythaemia can also occur after any subsequent increase in testosterone dose, switching from topical to parenteral administration and, development of comorbidity, which can be linked to an increase in haematocrit (e.g., respiratory or haematological diseases).

There is no evidence that an increase of haematocrit up to and including 54% causes any adverse effects. If the haematocrit exceeds 54% there is a testosterone independent, but weak associated rise in CV events and mortality [79, 177-179]. Any relationship is complex as these studies were based on patients with any cause of secondary polycythaemia, which included smoking and respiratory diseases. There have been no specific studies in men with only testosterone-induced erythrocytosis.

As detailed, the TRAVERSE study, which had included symptomatic hypogonadal men aged 45-80 years who had pre-existing or a high risk of CVD, showed a mild higher incidence of pulmonary embolism, a component of the adjudicated tertiary end point of venous thromboembolic events, in the testosterone therapy than in the placebo group (0.9% vs. 0.5%) [77]. However, three previous large studies have not shown any evidence that testosterone therapy is associated with an increased risk of venous thromboembolism [180, 181]. Of those, one study showed that an increased risk peaked at six months after initiation of testosterone therapy, and then declined over the subsequent period [182]. In one study venous thromboembolism was reported in 42 cases and 40 of these had a diagnosis of an underlying congenital thrombophilia (including factor V Leiden deficiency, prothrombin mutations and homocysteinuria) [183]. A meta-analysis of RCTs of testosterone therapy reported that venous thromboembolism was frequently related to underlying undiagnosed thrombophilia-hypofibrinolysis disorders [78]. In an RCT of testosterone therapy in men with chronic stable angina there were no adverse effects on coagulation, by assessment of tissue plasminogen activator or plasminogen activator inhibitor-1 enzyme activity or fibrinogen levels [184]. Similarly, another meta-analysis and systematic review of RCTs found that testosterone therapy was not associated with an increased risk of venous thromboembolism [164]. With testosterone therapy elevated haematocrit levels are more likely to occur if the baseline level is toward the upper limit of normal prior to initiation. Added risks for raised haematocrit on testosterone therapy include smoking or respiratory conditions at baseline. Higher haematocrit is more common with parenteral rather than topical formulations. Accordingly, a large retrospective two-arm open registry, comparing the effects of long-acting testosterone undecanoate and testosterone gels showed that the former preparation was associated with a higher risk of haematocrit levels > 50%, when compared to testosterone gels [185]. In men with pre-existing CVD extra caution is advised with a definitive diagnosis of hypogonadism before initiating testosterone therapy and monitoring of testosterone as well as haematocrit during treatment.

Elevated haematocrit in the absence of comorbidity or acute CV or venous thromboembolism can be managed by a reduction in testosterone dose, change in formulation or if the elevated haematocrit is very high by venesection (500 mL), even repeated if necessary, with usually no need to stop the testosterone therapy.

Thread 'Management of Erythrocytosis in Men Receiving TRT'

Nov 11, 2022

Management of Erythrocytosis in Men Receiving Testosterone Therapy: Clinical Consultation Guide (2022)
Pranjal Agrawal, Sajya M. Singh, Taylor Kohn


1. Introduction

Testosterone deficiency, previously known as male hypogonadism, affects approximately 25% of all men, with a prevalence that increases with age [1]. Risk factors for developing adult-onset testosterone deficiency include obesity, chronic disease, and poor general health [2]. Individuals with clinical hypogonadal symptoms and two-morning samples demonstrating low testosterone levels often...

• madman
• testosterone therapy; erythrocytosis
• Replies: 2
• Forum: Testosterone Side Effect Management

One of the more recent papers!

Professor Michael Zitzmann

We also know hematocrit can be increased by testosterone preparations. It depends on the preparation, and we think that there is data that shows that the threshold of 52-54% should not be surpassed, and men should be controlled for the hematocrit especially in the first year of treatment every 3 months



Hematocrit & Thromboembolic Risk

* TTh increase Hematocrit - clinically relevant at >52-54%

* Recommended: Control Hematocrit every 3 months in the 1st year

Thread 'TESTOSTERONE: A SAFETY UPDATE 2025'

Nov 16, 2025

Professor Michael Zitzmann

We also know hematocrit can be increased by testosterone preparations. It depends on the preparation, and we think that there is data that shows that the threshold of 52-54% should not be surpassed, and men should be controlled for the hematocrit especially in the first year of treatment every 3 months



Hematocrit & Thromboembolic Risk

* TTh increase Hematocrit - clinically relevant at >52-54%

* Recommended: Control Hematocrit every 3 months in the 1st year

...

• madman
• hypogonadism; testosterone; trt; cvd
• Replies: 25
• Forum: Testosterone and Men's Health Articles

 

[Funkybeats]

I've had 2 Oncologists/Hematologists put in writing that my Clinic should allow me 55% before donation. But, the Clinic is bound to Stone age protocols and refuse to allow me refills above 50%... Truly sucks. It totally F's my Iron and Ferritin #'s and pretty much negates much of the benefits of TRT.


Your provider clearly has no experience at this when it comes to those outdated stone-aged protocols or addressing elevated hematocrit if it creeps above 50%.

Find a new provider and get off that donating merry go round.




So, given everything I've learned, hypoxia is a main driver of high Hb and Hct and TRT is secondary.


Testosterone itself is a potent dose-dependent stimulus for erythropoiesis.

Many men who develop elevated Hct on T therapy do not have a significant hypoxic driver and even when factors such as OSA, obesity, smoking, or altitude are present maintaining chronically high FT levels especially high trough/steady-state FT provides a substantial erythropoietic stimulus.

I think T therapy and hypoxia are best viewed as additive factors but keep in mind when free T is maintained well above physiologic levels the androgen exposure itself can be the major driver of hematocrit elevation in many men.

Underlying hypoxic conditions can further amplify the response and are especially relevant in those who develop more significant elevations.

As I have stated numerous times on the forum it's not just the supraphysiologic peaks that have an impact on driving up the hematocrit as running too high a trough/steady-state FT will have a huge impact on pushing up the hematocrit.

Unfortunately too many men especially the ones caught up on that more T is better mentality bulls**t being pushed by all those sheep stinking up those so called mens health/HRT forums are running a very high trough FT as in levels that are elevated 24/7 steady-state.

The body was never meant to be amped up on T day in and day out 24/7.

Even if you move to more frequent injections as in dailies to clip the peak--->trough (minimal) and to maintain more stable blood levels throughout the week one can easily still struggle with elevated. hematocrit if they are still running too high a steady-state FT level.

In a patient without significant underlying risk factors such as untreated OSA, chronic hypoxia, smoking, uncontrolled hypertension, or CVD who is otherwise tolerating T therapy well many experienced clinicians would not automatically panic over a stable hematocrit around 50–54%.

They would assess the entire clinical picture including symptoms, trends, TT/FT levels, dosing, BP and potential contributors rather than treating the hematocrit value in isolation.



* No evidence of increased risk when elevated hematocrit is due to TTh

* Erythrocytosis suggests a possible cause of VTE and CV events with TTh, however no evidence of any association

* The hematocrit level at which the risk of neuro-occlusive events or cardiovascular events increases is not known

* Implication - 54% is an arbitrary cut-off

* The frequency of neuro-occlusive events in men with hypogonadism enrolled in RCTs of T who developed erythrocytosis has been very low

* Implications - little evidence of actual vascular risks associated with elevated hematocrit




What's that Abe?

* 54% is a useful, reasonable upper limit of acceptability


Come again, say it ain't so Abe!

* NO NEED TO INTERVENE unless HCT >54%

Thread 'Testosterone Therapy and erythrocytosis'

Jun 20, 2023

Testosterone Therapy and Men’s Health – Demystifying the Hype with Science to Provide Cutting-Edge Treatment for Your Patients (2021)

Summary 25:10-43:34 (Endocrine Society 2018 Guidelines)

Other Risks with Testosterone Therapy and How to Manage Them - T4L Education

t4leducation.com

• madman
• trt; erythrocytosis; hematocrit
• Replies: 7
• Forum: Testosterone Side Effect Management

• 

Sit back and dwell on this one!

*There is no evidence that an increase of haematocrit up to and including 54% causes any adverse effects. If the haematocrit exceeds 54% there is a testosterone independent, but weak associated rise in CV events and mortality [79, 177-179]. Any relationship is complex as these studies were based on patients with any cause of secondary polycythaemia, which included smoking and respiratory diseases. There have been no specific studies in men with only testosterone-induced erythrocytosis

Thread 'Transformative Insights from the Landmark Traverse Trial: A new era in testosterone therapy'

Apr 26, 2024

Nelson's house is where it's at!

• madman
• traverse; testosterone therapy; pca/cvd
• Replies: 22
• Forum: Testosterone and Men's Health Articles

• 

Some key takeaways here:

Cardiovascular Disease (CVD)

*Current available data from interventional studies suggest that there is no increased risk up to three years of testosterone therapy [167-171]. The currently published evidence has reported that testosterone therapy in men with diagnosed hypogonadism has neutral or beneficial actions on MACE in patients with normalised testosterone levels. The findings could be considered sufficiently reliable for at least a three year course of testosterone therapy, after which no available study can exclude further or long-term CV events [172,173]


Erythrocytosis

*There is no evidence that an increase of haematocrit up to and including 54% causes any adverse effects. If the haematocrit exceeds 54% there is a testosterone independent, but weak associated rise in CV events and mortality [79, 177-179]. Any relationship is complex as these studies were based on patients with any cause of secondary polycythaemia, which included smoking and respiratory diseases. There have been no specific studies in men with only testosterone-induced erythrocytosis.




EAU GUIDELINES ON SEXUAL AND REPRODUCTIVE HEALTH - LIMITED UPDATE APRIL 2024


3.5 Safety and follow-up in hypogonadism management


3.5.5 Cardiovascular Disease

Evidence suggests that hypogonadal men have an increased risk of CVD [146, 147]. Whether or not LOH is a cause or a consequence of atherosclerosis has not been clearly determined. Late-onset hypogonadism is associated with CV risk factors, including central obesity, insulin resistance and hyperglycaemia, dyslipidaemia, pro-thrombotic tendency and chronic inflammatory state [147]. Atherosclerosis is a chronic inflammatory disease, that releases pro-inflammatory cytokines into the circulation, which are known to suppress testosterone release from the HPG axis. Evidence from RCTs of testosterone therapy in men with MetS and/or T2DM demonstrates some benefit in CV risk, including reduced central adiposity, insulin resistance, total cholesterol and LDL-cholesterol and suppression of circulating cytokines [28-30, 35, 147, 148]. However, due to the equivocal nature of these studies, testosterone therapy cannot be recommended for use outside of treatment of specific symptoms.

Published data show that LOH is associated with an increase in all-cause and CVD-related mortality [7, 149-152]. These studies are supported by a meta-analysis that concluded that hypogonadism is a risk factor for cardiovascular morbidity [136] and mortality [153]. Importantly, men with low testosterone when compared to eugonadal men with angiographically proven coronary disease have twice the risk of earlier death [147]. Longitudinal population studies have reported that men with testosterone in the upper quartile of the normal range have a reduced number of CV events compared to men with testosterone in the lower three quartiles[149]. Androgen deprivation therapy for PCa is linked to an increased risk of CVD and sudden death [154].Conversely, two long-term epidemiological studies have reported reduced CV events in men with high normal serum testosterone levels [155, 156]. Erectile dysfunction is independently associated with CVD and may be the first clinical presentation in men with atherosclerosis.

The knowledge that men with hypogonadism and/or ED may have underlying CVD should prompt individual assessment of their CV risk profile. Individual risk factors (e.g., lifestyle, diet, exercise, smoking, hypertension,diabetes and dyslipidaemia) should be assessed and treated in men with pre-existing CVD and in patients receiving androgen deprivation therapy. Cardiovascular risk reduction can be managed by primary care clinicians, but patients should be appropriately counselled by clinicians active in prescribing testosterone therapy [83]. If appropriate, patients should be referred to cardiologists for risk stratification and treatment of comorbidity.

No RCTs have provided a clear answer on whether testosterone therapy affects CV outcomes. The TTrial (n=790) conducted in older men [157], the TIMES2 study (n=220) [29], along with the BLAST studies involving men with Metabolic Syndrome (MetS) and Type 2 Diabetes Mellitus (T2DM), as well as the study involving pre-frail and frail elderly men - all of which lasted for one year, and the T4DM study spanning two years - did not show any increase in Major Adverse Cardiovascular Events (MACE) increase in Major Adverse Cardiovascular Events (MACE) [29,32, 33, 157, 158]. Randomised controlled trials, between three and twelve months, in men with known heart disease treated with testosterone have not found an increase in MACE, but have reported improvement in cardiac ischaemia, angina and functional exercise capacity [159-161]. A large cohort study (n=20,4857 men) found that neither transdermal gel or intramuscular testosterone was associated with an increased risk of composite cardiovascular outcome in men with or without prevalent CVD (mean follow-up 4.3 years) [162]. The European Medicines Agency (EMA) has stated that ‘The Co-ordination Group for Mutual recognition and Decentralisation Procedures-Human (CMDh), a regulatory body representing EU Member States, has agreed by consensus that there is no consistent evidence of an increased risk of heart problems with testosterone in men. However, the product information is to be updated in line with the most current available evidence on safety, and with warnings that the lack of testosterone should be confirmed by signs and symptoms and laboratory tests before treating men with these drugs [163].

Data recently released from the TRAVERSE study confirm the findings of the EMA [77]. The latter is the first double-blind, placebo-controlled, non-inferiority RCT with primary CV safety as an end point. The results showed that testosterone therapy was noninferior to placebo with respect to the incidence of MACE. However, a mild higher incidence of atrial fibrillation, acute kidney injury, and pulmonary embolism was observed in the testosterone group [77]. The latter observations, however, need to be confirmed since previous available data do not support an increased risk of venous thromboembolism [78, 164] or major arrhythmias [165] after testosterone therapy. Similarly, the long-term follow-up (median of 5.1 years since last injection) of the T4DM study showed no differences in self-reported rates of new diagnosis of CVD [166].

In conclusion, current available data from interventional studies suggest that there is no increased risk up to three years of testosterone therapy [167-171]. The currently published evidence has reported that testosterone therapy in men with diagnosed hypogonadism has neutral or beneficial actions on MACE in patients with normalised testosterone levels. The findings could be considered sufficiently reliable for at least a three year course of testosterone therapy, after which no available study can exclude further or long-term CV events [172,173].




3.5.5.1 Cardiac Failure

Testosterone therapy is contraindicated in men with severe chronic cardiac failure because fluid retention may lead to exacerbation of the condition. Some studies have shown that men with moderate chronic cardiac failure may benefit from low doses of testosterone, which achieve mid-normal range testosterone levels [160,174, 175]. An interesting observation is that untreated hypogonadism increased the re-admission and mortality rate in men with heart failure [176]. If a decision is made to treat hypogonadism in men with chronic cardiac failure, it is essential that the patient is followed up carefully with clinical assessment and both testosterone and haematocrit measurements on a regular basis.




3.5.6 Erythrocytosis

An elevated haematocrit level is the most common adverse effect of testosterone therapy. Stimulation of erythropoiesis is a normal biological action that enhances the delivery of oxygen to testosterone-sensitive tissues (e.g., striated, smooth and cardiac muscle). Any elevation above the normal range for haematocrit usually becomes evident between three and twelve months after testosterone therapy initiation. However,polycythaemia can also occur after any subsequent increase in testosterone dose, switching from topical to parenteral administration and, development of comorbidity, which can be linked to an increase in haematocrit (e.g., respiratory or haematological diseases).

There is no evidence that an increase of haematocrit up to and including 54% causes any adverse effects. If the haematocrit exceeds 54% there is a testosterone independent, but weak associated rise in CV events and mortality [79, 177-179]. Any relationship is complex as these studies were based on patients with any cause of secondary polycythaemia, which included smoking and respiratory diseases. There have been no specific studies in men with only testosterone-induced erythrocytosis.

As detailed, the TRAVERSE study, which had included symptomatic hypogonadal men aged 45-80 years who had pre-existing or a high risk of CVD, showed a mild higher incidence of pulmonary embolism, a component of the adjudicated tertiary end point of venous thromboembolic events, in the testosterone therapy than in the placebo group (0.9% vs. 0.5%) [77]. However, three previous large studies have not shown any evidence that testosterone therapy is associated with an increased risk of venous thromboembolism [180, 181]. Of those, one study showed that an increased risk peaked at six months after initiation of testosterone therapy, and then declined over the subsequent period [182]. In one study venous thromboembolism was reported in 42 cases and 40 of these had a diagnosis of an underlying congenital thrombophilia (including factor V Leiden deficiency, prothrombin mutations and homocysteinuria) [183]. A meta-analysis of RCTs of testosterone therapy reported that venous thromboembolism was frequently related to underlying undiagnosed thrombophilia-hypofibrinolysis disorders [78]. In an RCT of testosterone therapy in men with chronic stable angina there were no adverse effects on coagulation, by assessment of tissue plasminogen activator or plasminogen activator inhibitor-1 enzyme activity or fibrinogen levels [184]. Similarly, another meta-analysis and systematic review of RCTs found that testosterone therapy was not associated with an increased risk of venous thromboembolism [164]. With testosterone therapy elevated haematocrit levels are more likely to occur if the baseline level is toward the upper limit of normal prior to initiation. Added risks for raised haematocrit on testosterone therapy include smoking or respiratory conditions at baseline. Higher haematocrit is more common with parenteral rather than topical formulations. Accordingly, a large retrospective two-arm open registry, comparing the effects of long-acting testosterone undecanoate and testosterone gels showed that the former preparation was associated with a higher risk of haematocrit levels > 50%, when compared to testosterone gels [185]. In men with pre-existing CVD extra caution is advised with a definitive diagnosis of hypogonadism before initiating testosterone therapy and monitoring of testosterone as well as haematocrit during treatment.

Elevated haematocrit in the absence of comorbidity or acute CV or venous thromboembolism can be managed by a reduction in testosterone dose, change in formulation or if the elevated haematocrit is very high by venesection (500 mL), even repeated if necessary, with usually no need to stop the testosterone therapy.

Thread 'Management of Erythrocytosis in Men Receiving TRT'

Nov 11, 2022

Management of Erythrocytosis in Men Receiving Testosterone Therapy: Clinical Consultation Guide (2022)
Pranjal Agrawal, Sajya M. Singh, Taylor Kohn


1. Introduction

Testosterone deficiency, previously known as male hypogonadism, affects approximately 25% of all men, with a prevalence that increases with age [1]. Risk factors for developing adult-onset testosterone deficiency include obesity, chronic disease, and poor general health [2]. Individuals with clinical hypogonadal symptoms and two-morning samples demonstrating low testosterone levels often...

• madman
• testosterone therapy; erythrocytosis
• Replies: 2
• Forum: Testosterone Side Effect Management

One of the more recent papers!

Professor Michael Zitzmann

We also know hematocrit can be increased by testosterone preparations. It depends on the preparation, and we think that there is data that shows that the threshold of 52-54% should not be surpassed, and men should be controlled for the hematocrit especially in the first year of treatment every 3 months



Hematocrit & Thromboembolic Risk

* TTh increase Hematocrit - clinically relevant at >52-54%

* Recommended: Control Hematocrit every 3 months in the 1st year

Thread 'TESTOSTERONE: A SAFETY UPDATE 2025'

Nov 16, 2025

Professor Michael Zitzmann

We also know hematocrit can be increased by testosterone preparations. It depends on the preparation, and we think that there is data that shows that the threshold of 52-54% should not be surpassed, and men should be controlled for the hematocrit especially in the first year of treatment every 3 months



Hematocrit & Thromboembolic Risk

* TTh increase Hematocrit - clinically relevant at >52-54%

* Recommended: Control Hematocrit every 3 months in the 1st year

...

• madman
• hypogonadism; testosterone; trt; cvd
• Replies: 25
• Forum: Testosterone and Men's Health Articles

Hey Madman,

Do you know of any studies that look at HCT as a confounding factor to individuals with a high Lp(a)? I think it would be obvious that the two together would increase CVD risk but was wondering if there's any data on it that would suggest a lower cutoff for intervention on HCT for men in TRT with high Lp(a).

 

[Leeman]

I've had 2 Oncologists/Hematologists put in writing that my Clinic should allow me 55% before donation. But, the Clinic is bound to Stone age protocols and refuse to allow me refills above 50%... Truly sucks. It totally F's my Iron and Ferritin #'s and pretty much negates much of the benefits of TRT.


Your provider clearly has no experience at this when it comes to those outdated stone-aged protocols or addressing elevated hematocrit if it creeps above 50%.

Find a new provider and get off that donating merry go round.




So, given everything I've learned, hypoxia is a main driver of high Hb and Hct and TRT is secondary.


Testosterone itself is a potent dose-dependent stimulus for erythropoiesis.

Many men who develop elevated Hct on T therapy do not have a significant hypoxic driver and even when factors such as OSA, obesity, smoking, or altitude are present maintaining chronically high FT levels especially high trough/steady-state FT provides a substantial erythropoietic stimulus.

I think T therapy and hypoxia are best viewed as additive factors but keep in mind when free T is maintained well above physiologic levels the androgen exposure itself can be the major driver of hematocrit elevation in many men.

Underlying hypoxic conditions can further amplify the response and are especially relevant in those who develop more significant elevations.

As I have stated numerous times on the forum it's not just the supraphysiologic peaks that have an impact on driving up the hematocrit as running too high a trough/steady-state FT will have a huge impact on pushing up the hematocrit.

Unfortunately too many men especially the ones caught up on that more T is better mentality bulls**t being pushed by all those sheep stinking up those so called mens health/HRT forums are running a very high trough FT as in levels that are elevated 24/7 steady-state.

The body was never meant to be amped up on T day in and day out 24/7.

Even if you move to more frequent injections as in dailies to clip the peak--->trough (minimal) and to maintain more stable blood levels throughout the week one can easily still struggle with elevated. hematocrit if they are still running too high a steady-state FT level.

In a patient without significant underlying risk factors such as untreated OSA, chronic hypoxia, smoking, uncontrolled hypertension, or CVD who is otherwise tolerating T therapy well many experienced clinicians would not automatically panic over a stable hematocrit around 50–54%.

They would assess the entire clinical picture including symptoms, trends, TT/FT levels, dosing, BP and potential contributors rather than treating the hematocrit value in isolation.



* No evidence of increased risk when elevated hematocrit is due to TTh

* Erythrocytosis suggests a possible cause of VTE and CV events with TTh, however no evidence of any association

* The hematocrit level at which the risk of neuro-occlusive events or cardiovascular events increases is not known

* Implication - 54% is an arbitrary cut-off

* The frequency of neuro-occlusive events in men with hypogonadism enrolled in RCTs of T who developed erythrocytosis has been very low

* Implications - little evidence of actual vascular risks associated with elevated hematocrit




What's that Abe?

* 54% is a useful, reasonable upper limit of acceptability


Come again, say it ain't so Abe!

* NO NEED TO INTERVENE unless HCT >54%

Thread 'Testosterone Therapy and erythrocytosis'

Jun 20, 2023

Testosterone Therapy and Men’s Health – Demystifying the Hype with Science to Provide Cutting-Edge Treatment for Your Patients (2021)

Summary 25:10-43:34 (Endocrine Society 2018 Guidelines)

Other Risks with Testosterone Therapy and How to Manage Them - T4L Education

t4leducation.com

• madman
• trt; erythrocytosis; hematocrit
• Replies: 7
• Forum: Testosterone Side Effect Management

• 

Sit back and dwell on this one!

*There is no evidence that an increase of haematocrit up to and including 54% causes any adverse effects. If the haematocrit exceeds 54% there is a testosterone independent, but weak associated rise in CV events and mortality [79, 177-179]. Any relationship is complex as these studies were based on patients with any cause of secondary polycythaemia, which included smoking and respiratory diseases. There have been no specific studies in men with only testosterone-induced erythrocytosis

Thread 'Transformative Insights from the Landmark Traverse Trial: A new era in testosterone therapy'

Apr 26, 2024

Nelson's house is where it's at!

• madman
• traverse; testosterone therapy; pca/cvd
• Replies: 22
• Forum: Testosterone and Men's Health Articles

• 

Some key takeaways here:

Cardiovascular Disease (CVD)

*Current available data from interventional studies suggest that there is no increased risk up to three years of testosterone therapy [167-171]. The currently published evidence has reported that testosterone therapy in men with diagnosed hypogonadism has neutral or beneficial actions on MACE in patients with normalised testosterone levels. The findings could be considered sufficiently reliable for at least a three year course of testosterone therapy, after which no available study can exclude further or long-term CV events [172,173]


Erythrocytosis

*There is no evidence that an increase of haematocrit up to and including 54% causes any adverse effects. If the haematocrit exceeds 54% there is a testosterone independent, but weak associated rise in CV events and mortality [79, 177-179]. Any relationship is complex as these studies were based on patients with any cause of secondary polycythaemia, which included smoking and respiratory diseases. There have been no specific studies in men with only testosterone-induced erythrocytosis.




EAU GUIDELINES ON SEXUAL AND REPRODUCTIVE HEALTH - LIMITED UPDATE APRIL 2024


3.5 Safety and follow-up in hypogonadism management


3.5.5 Cardiovascular Disease

Evidence suggests that hypogonadal men have an increased risk of CVD [146, 147]. Whether or not LOH is a cause or a consequence of atherosclerosis has not been clearly determined. Late-onset hypogonadism is associated with CV risk factors, including central obesity, insulin resistance and hyperglycaemia, dyslipidaemia, pro-thrombotic tendency and chronic inflammatory state [147]. Atherosclerosis is a chronic inflammatory disease, that releases pro-inflammatory cytokines into the circulation, which are known to suppress testosterone release from the HPG axis. Evidence from RCTs of testosterone therapy in men with MetS and/or T2DM demonstrates some benefit in CV risk, including reduced central adiposity, insulin resistance, total cholesterol and LDL-cholesterol and suppression of circulating cytokines [28-30, 35, 147, 148]. However, due to the equivocal nature of these studies, testosterone therapy cannot be recommended for use outside of treatment of specific symptoms.

Published data show that LOH is associated with an increase in all-cause and CVD-related mortality [7, 149-152]. These studies are supported by a meta-analysis that concluded that hypogonadism is a risk factor for cardiovascular morbidity [136] and mortality [153]. Importantly, men with low testosterone when compared to eugonadal men with angiographically proven coronary disease have twice the risk of earlier death [147]. Longitudinal population studies have reported that men with testosterone in the upper quartile of the normal range have a reduced number of CV events compared to men with testosterone in the lower three quartiles[149]. Androgen deprivation therapy for PCa is linked to an increased risk of CVD and sudden death [154].Conversely, two long-term epidemiological studies have reported reduced CV events in men with high normal serum testosterone levels [155, 156]. Erectile dysfunction is independently associated with CVD and may be the first clinical presentation in men with atherosclerosis.

The knowledge that men with hypogonadism and/or ED may have underlying CVD should prompt individual assessment of their CV risk profile. Individual risk factors (e.g., lifestyle, diet, exercise, smoking, hypertension,diabetes and dyslipidaemia) should be assessed and treated in men with pre-existing CVD and in patients receiving androgen deprivation therapy. Cardiovascular risk reduction can be managed by primary care clinicians, but patients should be appropriately counselled by clinicians active in prescribing testosterone therapy [83]. If appropriate, patients should be referred to cardiologists for risk stratification and treatment of comorbidity.

No RCTs have provided a clear answer on whether testosterone therapy affects CV outcomes. The TTrial (n=790) conducted in older men [157], the TIMES2 study (n=220) [29], along with the BLAST studies involving men with Metabolic Syndrome (MetS) and Type 2 Diabetes Mellitus (T2DM), as well as the study involving pre-frail and frail elderly men - all of which lasted for one year, and the T4DM study spanning two years - did not show any increase in Major Adverse Cardiovascular Events (MACE) increase in Major Adverse Cardiovascular Events (MACE) [29,32, 33, 157, 158]. Randomised controlled trials, between three and twelve months, in men with known heart disease treated with testosterone have not found an increase in MACE, but have reported improvement in cardiac ischaemia, angina and functional exercise capacity [159-161]. A large cohort study (n=20,4857 men) found that neither transdermal gel or intramuscular testosterone was associated with an increased risk of composite cardiovascular outcome in men with or without prevalent CVD (mean follow-up 4.3 years) [162]. The European Medicines Agency (EMA) has stated that ‘The Co-ordination Group for Mutual recognition and Decentralisation Procedures-Human (CMDh), a regulatory body representing EU Member States, has agreed by consensus that there is no consistent evidence of an increased risk of heart problems with testosterone in men. However, the product information is to be updated in line with the most current available evidence on safety, and with warnings that the lack of testosterone should be confirmed by signs and symptoms and laboratory tests before treating men with these drugs [163].

Data recently released from the TRAVERSE study confirm the findings of the EMA [77]. The latter is the first double-blind, placebo-controlled, non-inferiority RCT with primary CV safety as an end point. The results showed that testosterone therapy was noninferior to placebo with respect to the incidence of MACE. However, a mild higher incidence of atrial fibrillation, acute kidney injury, and pulmonary embolism was observed in the testosterone group [77]. The latter observations, however, need to be confirmed since previous available data do not support an increased risk of venous thromboembolism [78, 164] or major arrhythmias [165] after testosterone therapy. Similarly, the long-term follow-up (median of 5.1 years since last injection) of the T4DM study showed no differences in self-reported rates of new diagnosis of CVD [166].

In conclusion, current available data from interventional studies suggest that there is no increased risk up to three years of testosterone therapy [167-171]. The currently published evidence has reported that testosterone therapy in men with diagnosed hypogonadism has neutral or beneficial actions on MACE in patients with normalised testosterone levels. The findings could be considered sufficiently reliable for at least a three year course of testosterone therapy, after which no available study can exclude further or long-term CV events [172,173].




3.5.5.1 Cardiac Failure

Testosterone therapy is contraindicated in men with severe chronic cardiac failure because fluid retention may lead to exacerbation of the condition. Some studies have shown that men with moderate chronic cardiac failure may benefit from low doses of testosterone, which achieve mid-normal range testosterone levels [160,174, 175]. An interesting observation is that untreated hypogonadism increased the re-admission and mortality rate in men with heart failure [176]. If a decision is made to treat hypogonadism in men with chronic cardiac failure, it is essential that the patient is followed up carefully with clinical assessment and both testosterone and haematocrit measurements on a regular basis.




3.5.6 Erythrocytosis

An elevated haematocrit level is the most common adverse effect of testosterone therapy. Stimulation of erythropoiesis is a normal biological action that enhances the delivery of oxygen to testosterone-sensitive tissues (e.g., striated, smooth and cardiac muscle). Any elevation above the normal range for haematocrit usually becomes evident between three and twelve months after testosterone therapy initiation. However,polycythaemia can also occur after any subsequent increase in testosterone dose, switching from topical to parenteral administration and, development of comorbidity, which can be linked to an increase in haematocrit (e.g., respiratory or haematological diseases).

There is no evidence that an increase of haematocrit up to and including 54% causes any adverse effects. If the haematocrit exceeds 54% there is a testosterone independent, but weak associated rise in CV events and mortality [79, 177-179]. Any relationship is complex as these studies were based on patients with any cause of secondary polycythaemia, which included smoking and respiratory diseases. There have been no specific studies in men with only testosterone-induced erythrocytosis.

As detailed, the TRAVERSE study, which had included symptomatic hypogonadal men aged 45-80 years who had pre-existing or a high risk of CVD, showed a mild higher incidence of pulmonary embolism, a component of the adjudicated tertiary end point of venous thromboembolic events, in the testosterone therapy than in the placebo group (0.9% vs. 0.5%) [77]. However, three previous large studies have not shown any evidence that testosterone therapy is associated with an increased risk of venous thromboembolism [180, 181]. Of those, one study showed that an increased risk peaked at six months after initiation of testosterone therapy, and then declined over the subsequent period [182]. In one study venous thromboembolism was reported in 42 cases and 40 of these had a diagnosis of an underlying congenital thrombophilia (including factor V Leiden deficiency, prothrombin mutations and homocysteinuria) [183]. A meta-analysis of RCTs of testosterone therapy reported that venous thromboembolism was frequently related to underlying undiagnosed thrombophilia-hypofibrinolysis disorders [78]. In an RCT of testosterone therapy in men with chronic stable angina there were no adverse effects on coagulation, by assessment of tissue plasminogen activator or plasminogen activator inhibitor-1 enzyme activity or fibrinogen levels [184]. Similarly, another meta-analysis and systematic review of RCTs found that testosterone therapy was not associated with an increased risk of venous thromboembolism [164]. With testosterone therapy elevated haematocrit levels are more likely to occur if the baseline level is toward the upper limit of normal prior to initiation. Added risks for raised haematocrit on testosterone therapy include smoking or respiratory conditions at baseline. Higher haematocrit is more common with parenteral rather than topical formulations. Accordingly, a large retrospective two-arm open registry, comparing the effects of long-acting testosterone undecanoate and testosterone gels showed that the former preparation was associated with a higher risk of haematocrit levels > 50%, when compared to testosterone gels [185]. In men with pre-existing CVD extra caution is advised with a definitive diagnosis of hypogonadism before initiating testosterone therapy and monitoring of testosterone as well as haematocrit during treatment.

Elevated haematocrit in the absence of comorbidity or acute CV or venous thromboembolism can be managed by a reduction in testosterone dose, change in formulation or if the elevated haematocrit is very high by venesection (500 mL), even repeated if necessary, with usually no need to stop the testosterone therapy.

Thread 'Management of Erythrocytosis in Men Receiving TRT'

Nov 11, 2022

Management of Erythrocytosis in Men Receiving Testosterone Therapy: Clinical Consultation Guide (2022)
Pranjal Agrawal, Sajya M. Singh, Taylor Kohn


1. Introduction

Testosterone deficiency, previously known as male hypogonadism, affects approximately 25% of all men, with a prevalence that increases with age [1]. Risk factors for developing adult-onset testosterone deficiency include obesity, chronic disease, and poor general health [2]. Individuals with clinical hypogonadal symptoms and two-morning samples demonstrating low testosterone levels often...

• madman
• testosterone therapy; erythrocytosis
• Replies: 2
• Forum: Testosterone Side Effect Management

One of the more recent papers!

Professor Michael Zitzmann

We also know hematocrit can be increased by testosterone preparations. It depends on the preparation, and we think that there is data that shows that the threshold of 52-54% should not be surpassed, and men should be controlled for the hematocrit especially in the first year of treatment every 3 months



Hematocrit & Thromboembolic Risk

* TTh increase Hematocrit - clinically relevant at >52-54%

* Recommended: Control Hematocrit every 3 months in the 1st year

Thread 'TESTOSTERONE: A SAFETY UPDATE 2025'

Nov 16, 2025

Professor Michael Zitzmann

We also know hematocrit can be increased by testosterone preparations. It depends on the preparation, and we think that there is data that shows that the threshold of 52-54% should not be surpassed, and men should be controlled for the hematocrit especially in the first year of treatment every 3 months



Hematocrit & Thromboembolic Risk

* TTh increase Hematocrit - clinically relevant at >52-54%

* Recommended: Control Hematocrit every 3 months in the 1st year

...

• madman
• hypogonadism; testosterone; trt; cvd
• Replies: 25
• Forum: Testosterone and Men's Health Articles

Thank you!! Greatly appreciated.

Your provider clearly has no experience at this when it comes to those outdated stone-aged protocols or addressing elevated hematocrit if it creeps above 50%.

Find a new provider and get off that donating merry go round.

Agreed 100%. My Clinic is the Low T Center and they are a for profit only racket... (they were MUCH better 10yrs ago.) They've made a ton of regrettable changes to their practices and Business decisions.

GET THIS: They run the Clinics in many States, they do all the Lab's in house (in Tx) AND they compound their own Testosterone in Tx!
Where's the accountability? Where's the 3rd party anything?? Compounded pharmaceuticals are NOT bound to Federal Reg's, only State level Regulations...
I've had some VERY questionable Lab's via LTC.

My Hct is fairly stable @ 50-52% and has been for a few yrs. Granted, I'm not on 100mg p/wk! But, slowly titrated up over the yrs to a max of 220mg Cyp. (110/110) I've also titrated back down to 160mgs (80/80) p/wk with no appreciable difference in Hct.

Even worse, when my dose is down to 180 or less, I don't have good libido, night and morning wood, any real drive in the gym, (I normally Powerlift competitively) to name a few neg issues. (I'm @ 180/wk now. 60/60/60)

But, much of this "could" also be caused or exasperated by Chronic Low to mediocre Iron and Ferritin levels due to excess phlebotomies...

"The body was never meant to be amped up on T day in and day out 24/7."

I agree. I've always tried to keep the exogenous T to a minimum (Min Effective dose) and I never liked the idea of dosing every day to achieve a "steady state" 24/7. In theory it sounds great. But, the natural body does not maintain a perfect steady state level 24/7. There's a natural ebb & flow. Granted it's surely a 1000 times better than one bolus injection every 2 weeks!! Lol! But, for me I didn't feel better on it and it's kind of a PITA to have to do. (especially traveling, etc...) But, the main thing is being jacked up on it 24/7/365 with no natural ebb & flow. **purely just my personal opinion...

Madman, you had mentioned something about over taxing the CNS and Dopamine receptors somewhere and that hit home with me.

I have been telling my wife for a while now,(months!) how I just don't have any overdrive in the gym on big lift days and I rarely get up or excited about ANYTHING anymore, or for anything, like the Reward aspect of Dopamine just isn't there. Feels like my Dopamine is tapped out...

Could be many things combined, creating the perfect storm. But, to be honest, I'm quite concerned about it. If you have any more thoughts regarding T abuse crashing the CNS and/or Dopamine aspect, I'd love to hear it. I don't think I've totally abused TRT being under 200mg/wk. (I've spent more time under 200, than over 200 in the last 10yrs) But, maybe I have. Maybe my high demand Training, and Low Ferritin, etc... has also played a part?? I didn't get the phony Jab, so I can rule that out thankfully!

Thx again for your time and efforts on here

 

[madman]

Hey Madman,

Do you know of any studies that look at HCT as a confounding factor to individuals with a high Lp(a)? I think it would be obvious that the two together would increase CVD risk but was wondering if there's any data on it that would suggest a lower cutoff for intervention on HCT for men in TRT with high Lp(a).

Not aware of any.

This is where it stands as of now.

Key point here.

Some clinicians use 52% as a softer “watch and manage” threshold, particularly for men with additional cardiovascular risk factors.




* Most current guidelines, including those from the American Urological Association and the Endocrine Society, flag hematocrit above 54% as a threshold requiring intervention. Some clinicians use 52% as a softer “watch and manage” threshold, particularly for men with additional cardiovascular risk factors.


* It is important to say clearly: research on whether physiologic-dose TRT meaningfully increases cardiovascular risk is mixed. The large TRAVERSE trial, published in 2023, found that TRT in men with hypogonadism and elevated cardiovascular risk did not significantly increase major adverse cardiovascular events (MACE) compared to placebo. But that finding applies to well-monitored, physiologic dosing. It does not apply to men whose hematocrit climbs above 54–55% without intervention.


* Men with additional risk factors (history of DVT or PE, sleep apnea, COPD, obesity, or a family history of clotting disorders) should recheck more frequently: every 3 months until the hematocrit trend is stable.

Thread 'High Hematocrit on TRT: practical “numbers plus action” guide'

Feb 24, 2026

How often should men on TRT check their hematocrit?​

The standard monitoring schedule includes a baseline CBC before starting TRT, a recheck at 3 to 6 weeks, another at 3 months, and then at 6 and 12 months once stable. Any dose or formulation change resets the monitoring clock, requiring a recheck 4 to 6 weeks later. Men with risk factors for elevated hematocrit (sleep apnea, smoking, COPD, or a history of clotting) should check more frequently: every 3 months until the trend is stable.




* The monitoring schedule, the intervention ladder, and the attention...

• madman
• hypogonadism; t-therapy; hematocrit; cvd
• Replies: 6
• Forum: Testosterone Side Effect Management

 

[madman]

Thank you!! Greatly appreciated.

Your provider clearly has no experience at this when it comes to those outdated stone-aged protocols or addressing elevated hematocrit if it creeps above 50%.

Find a new provider and get off that donating merry go round.

Agreed 100%. My Clinic is the Low T Center and they are a for profit only racket... (they were MUCH better 10yrs ago.) They've made a ton of regrettable changes to their practices and Business decisions.

GET THIS: They run the Clinics in many States, they do all the Lab's in house (in Tx) AND they compound their own Testosterone in Tx!
Where's the accountability? Where's the 3rd party anything?? Compounded pharmaceuticals are NOT bound to Federal Reg's, only State level Regulations...
I've had some VERY questionable Lab's via LTC.

My Hct is fairly stable @ 50-52% and has been for a few yrs. Granted, I'm not on 100mg p/wk! But, slowly titrated up over the yrs to a max of 220mg Cyp. (110/110) I've also titrated back down to 160mgs (80/80) p/wk with no appreciable difference in Hct.

Even worse, when my dose is down to 180 or less, I don't have good libido, night and morning wood, any real drive in the gym, (I normally Powerlift competitively) to name a few neg issues. (I'm @ 180/wk now. 60/60/60)

But, much of this "could" also be caused or exasperated by Chronic Low to mediocre Iron and Ferritin levels due to excess phlebotomies...

"The body was never meant to be amped up on T day in and day out 24/7."

I agree. I've always tried to keep the exogenous T to a minimum (Min Effective dose) and I never liked the idea of dosing every day to achieve a "steady state" 24/7. In theory it sounds great. But, the natural body does not maintain a perfect steady state level 24/7. There's a natural ebb & flow. Granted it's surely a 1000 times better than one bolus injection every 2 weeks!! Lol! But, for me I didn't feel better on it and it's kind of a PITA to have to do. (especially traveling, etc...) But, the main thing is being jacked up on it 24/7/365 with no natural ebb & flow. **purely just my personal opinion...

Madman, you had mentioned something about over taxing the CNS and Dopamine receptors somewhere and that hit home with me.

I have been telling my wife for a while now,(months!) how I just don't have any overdrive in the gym on big lift days and I rarely get up or excited about ANYTHING anymore, or for anything, like the Reward aspect of Dopamine just isn't there. Feels like my Dopamine is tapped out...

Could be many things combined, creating the perfect storm. But, to be honest, I'm quite concerned about it. If you have any more thoughts regarding T abuse crashing the CNS and/or Dopamine aspect, I'd love to hear it. I don't think I've totally abused TRT being under 200mg/wk. (I've spent more time under 200, than over 200 in the last 10yrs) But, maybe I have. Maybe my high demand Training, and Low Ferritin, etc... has also played a part?? I didn't get the phony Jab, so I can rule that out thankfully!

Thx again for your time and efforts on here

My Hct is fairly stable @ 50-52% and has been for a few yrs. Granted, I'm not on 100mg p/wk! But, slowly titrated up over the yrs to a max of 220mg Cyp. (110/110) I've also titrated back down to 160mgs (80/80) p/wk with no appreciable difference in Hct.


Hope you understand that it would take many months to see the true outcome when lowering the T dose and bringing down the trough/steady-state FT as the lifecycle of an RBC is 120 days.

Many do not give it enough time and end up jumping the gun too soon.








Even worse, when my dose is down to 180 or less, I don't have good libido, night and morning wood, any real drive in the gym, (I normally Powerlift competitively) to name a few neg issues. (I'm @ 180/wk now. 60/60/60)

But, much of this "could" also be caused or exasperated by Chronic Low to mediocre Iron and Ferritin levels due to excess phlebotomies...


Similar scenario here when lowering the dose and bringing down the trough/steady-state FT as hormones will be in FLUX during the weeks leading up until blood levels have stabilized (4-6 weeks TC/TE) and it. is common for one to experience bumps along the way especially when it comes to libido and erectile function as the body is trying to ADJUST to the declining T/metabolites.
Even then once blood levels have stabilized (4-6 weeks TC/TE) it will still take time as in a few more months for the body to ADAPT to its new SET-POINT and this is the critical time period one needs to gauge how they truly feel overall regarding relief/improvement of low-T symptoms and overall well-being.

Every protocol whether one is increasing or decreasing the dose of T needs to be given 12 weeks before claiming whether it was a success or failure.

This is where many men fail as they lack the understanding of how exogenous T works.

You need to give the protocol a fair shake before throwing in the towel.

Unfortunately too many men bail way too early when lowering the dose and end up jacking their FT levels up again.

The first 6 weeks means nothing when looking at the bigger picture here.

It is far from a given how you feel 6 weeks in is how you will feel 3-4 months later.

Patience is key here.

Unfortunately those who do not understand this are the ones tweaking their dose every 6-8 weeks because they do not feel well.

Keep in mind going up will always be easier than having to come down.

Even then libido/erectile function are both multi-factorial and having healthy T levels is only one piece of the puzzle.

Much more involved than just hormones.

Hope you understand that the threshold for erectile functions. is not that high as in well within the physiologic range and when it comes to libido its a myth that high FT or high DHT is needed.

All that truly matters here is having a healthy FT.

As I have stressed numerous times on the forum over the years.

Much more to the story when it comes to testosterones impact on libido/erectile function!


* Again having a healthy FT is only one piece of the puzzle as libido let alone ED are multifactorial.

* Getting quality sleep, minimizing stress (physical/mental), following a healthy diet, exercising/staying active, improving overall vascular health will have a far bigger impact than jacking up your trough FT!

* Have realistic expectations especially when it comes to libido and erectile function!

Post in thread 'Testosterone + Men's Sexual Health'

Nov 10, 2024

PURE MADNESS!

Much more to the story when it comes to testosterones impact on libido/erectile function!


*Again having a healthy FT is only one piece of the puzzle as libido let alone ED are multifactorial.

*Getting quality sleep, minimizing stress (physical/mental), following a healthy diet, exercising/staying active, improving overall vascular health will have a far bigger impact than jacking up your trough FT!

*Have realistic expectations especially when it comes to libido and erectile function!



LIBIDO...

• madman

Madman, you had mentioned something about over taxing the CNS and Dopamine receptors somewhere and that hit home with me.


Yes T has. a tonic effect on the CNS and running too high a trough/steady-state FT can easily have a negative impact on mood, energy, sleep quality, libido and erectile function especially when you are hammering the s**t out of your CNS/dopamine 24/7.

As I stated previously the body was never meant to be amped up on T day in day out 24/7.








Again would tread lightly on how high you run your trough/steady-state FT level!

This can easily backfire in the long-run for many especially when it comes to mood, libido and erectile function!

Too high a FT level can be just as bad in many ways as having too low a FT level.

Libido starts in the brain.

Neurotransmitters have a big impact especially dopamine.

There is a fine balance here when it comes to the dopamine system!

This is key here..... dopamine circuits are powerfully regulated by androgens!

Thread 'Androgen modulation of mesoprefrontal dopamine systems and the effects of these actions on the adult male brain'

Jul 13, 2024

Again would tread lightly on how high you run your trough/steady-state FT level!

This can easily backfire in the long-run for many especially when it comes to mood, libido and erectile function!

Too high a FT level can be just as bad in many ways as having too low a FT level.

Libido starts in the brain.

Neurotransmitters have a big impact especially dopamine.

There is a fine balance here when it comes to the dopamine system!

This is key here..... dopamine circuits are powerfully regulated by androgens!




*dopamine circuits are powerfully regulated by androgens...

• madman
• dopamine; testosterone; ar; cognition
• Replies: 12
• Forum: Testosterone and Men's Health Articles

• 

 

[Leeman]

My Hct is fairly stable @ 50-52% and has been for a few yrs. Granted, I'm not on 100mg p/wk! But, slowly titrated up over the yrs to a max of 220mg Cyp. (110/110) I've also titrated back down to 160mgs (80/80) p/wk with no appreciable difference in Hct.


Hope you understand that it would take many months to see the true outcome when lowering the T dose and bringing down the trough/steady-state FT as the lifecycle of an RBC is 120 days.

Many do not give it enough time and end up jumping the gun too soon.








Even worse, when my dose is down to 180 or less, I don't have good libido, night and morning wood, any real drive in the gym, (I normally Powerlift competitively) to name a few neg issues. (I'm @ 180/wk now. 60/60/60)

But, much of this "could" also be caused or exasperated by Chronic Low to mediocre Iron and Ferritin levels due to excess phlebotomies...


Similar scenario here when lowering the dose and bringing down the trough/steady-state FT as hormones will be in FLUX during the weeks leading up until blood levels have stabilized (4-6 weeks TC/TE) and it. is common for one to experience bumps along the way especially when it comes to libido and erectile function as the body is trying to ADJUST to the declining T/metabolites.
Even then once blood levels have stabilized (4-6 weeks TC/TE) it will still take time as in a few more months for the body to ADAPT to its new SET-POINT and this is the critical time period one needs to gauge how they truly feel overall regarding relief/improvement of low-T symptoms and overall well-being.

Every protocol whether one is increasing or decreasing the dose of T needs to be given 12 weeks before claiming whether it was a success or failure.

This is where many men fail as they lack the understanding of how exogenous T works.

You need to give the protocol a fair shake before throwing in the towel.

Unfortunately too many men bail way too early when lowering the dose and end up jacking their FT levels up again.

The first 6 weeks means nothing when looking at the bigger picture here.

It is far from a given how you feel 6 weeks in is how you will feel 3-4 months later.

Patience is key here.

Unfortunately those who do not understand this are the ones tweaking their dose every 6-8 weeks because they do not feel well.

Keep in mind going up will always be easier than having to come down.

Even then libido/erectile function are both multi-factorial and having healthy T levels is only one piece of the puzzle.

Much more involved than just hormones.

Hope you understand that the threshold for erectile functions. is not that high as in well within the physiologic range and when it comes to libido its a myth that high FT or high DHT is needed.

All that truly matters here is having a healthy FT.

As I have stressed numerous times on the forum over the years.

Much more to the story when it comes to testosterones impact on libido/erectile function!


* Again having a healthy FT is only one piece of the puzzle as libido let alone ED are multifactorial.

* Getting quality sleep, minimizing stress (physical/mental), following a healthy diet, exercising/staying active, improving overall vascular health will have a far bigger impact than jacking up your trough FT!

* Have realistic expectations especially when it comes to libido and erectile function!

Post in thread 'Testosterone + Men's Sexual Health'

Nov 10, 2024

PURE MADNESS!

Much more to the story when it comes to testosterones impact on libido/erectile function!


*Again having a healthy FT is only one piece of the puzzle as libido let alone ED are multifactorial.

*Getting quality sleep, minimizing stress (physical/mental), following a healthy diet, exercising/staying active, improving overall vascular health will have a far bigger impact than jacking up your trough FT!

*Have realistic expectations especially when it comes to libido and erectile function!



LIBIDO...

• madman

Madman, you had mentioned something about over taxing the CNS and Dopamine receptors somewhere and that hit home with me.


Yes T has. a tonic effect on the CNS and running too high a trough/steady-state FT can easily have a negative impact on mood, energy, sleep quality, libido and erectile function especially when you are hammering the s**t out of your CNS/dopamine 24/7.

As I stated previously the body was never meant to be amped up on T day in day out 24/7.








Again would tread lightly on how high you run your trough/steady-state FT level!

This can easily backfire in the long-run for many especially when it comes to mood, libido and erectile function!

Too high a FT level can be just as bad in many ways as having too low a FT level.

Libido starts in the brain.

Neurotransmitters have a big impact especially dopamine.

There is a fine balance here when it comes to the dopamine system!

This is key here..... dopamine circuits are powerfully regulated by androgens!

Thread 'Androgen modulation of mesoprefrontal dopamine systems and the effects of these actions on the adult male brain'

Jul 13, 2024

Again would tread lightly on how high you run your trough/steady-state FT level!

This can easily backfire in the long-run for many especially when it comes to mood, libido and erectile function!

Too high a FT level can be just as bad in many ways as having too low a FT level.

Libido starts in the brain.

Neurotransmitters have a big impact especially dopamine.

There is a fine balance here when it comes to the dopamine system!

This is key here..... dopamine circuits are powerfully regulated by androgens!




*dopamine circuits are powerfully regulated by androgens...

• madman
• dopamine; testosterone; ar; cognition
• Replies: 12
• Forum: Testosterone and Men's Health Articles

• 

Awesome! Thx

Many Great points. I am probably guilty of jumping the gun a little a few times over the yrs. per the Clinic trying over come my negative symptoms which crept in after multi donations and with at least 3 product manufacturer changes. (this was before Low T Center began doing and compounding everything in house) Other than a few instances, I try really hard to stay incredibly consistent on dosages and injection frequency, with Lab's every 3 mon's. (with any changes in dosage amount being small and no sooner than 6-12wks)

(I've got every Lab since 2015) My 7 day trough TT in the last few yrs is typically 600-700 and Trough FT ave 19-20. I've had some VERY questionable Lab's with trough TT 900 to just over 1000, and FT @ 29 and 33. These were rogue values, with no explanation for the High #'s. Just as strange, are the Rogue Low values of 333 and 400 Trough TT and very Low trough FT #'s of 8-10.

Yrs ago, I could absolutely "Feel" High E2 in my nipples! (even slight sensitivity changes were evident) And I dosed Anastrozole .25-.50 p/wk to manage this and many other typical High E2 symptoms that might creep in. However, since getting off Olympia and Empower brands (from a vial) and going to LTC's Compounded "Franken-T", Nothing has ever been he same... Nothing is predictable anymore.

The main reason we titrated down, was to try to remove the need for any Anastrozole and to eliminate the need to Donate as frequently. His theory was; if you need an AI (at all) or need to Donate, your dosage is too high! ...I tried his "Theory" but, for me (at the time) it didn't help. I felt like shit and it didn't change my Hct levels. In fact, over the past 5-6 yrs, nothing has really ever changed my Hct #'s.

I will admit being below 220mg/wk does extend donations a little, E2 is much less of a challenge, sleep is better, and BP and HR are both lower. (FWIW, youthful libido and very dependable night/morn wood was much better @ 200-220mg/wk) But, I don't need to be that jacked up (hormonally) and animalistic at my age and married! Lol Never had any ED issues with High or Low T, THANKFULLY!! At worst, I feel like my refractory period might be 7-10 days and that just seems wrong!! Lol!! Where do I turn in my Man Card?!?!

I'd LOVE to not be on ANY AI what so ever (I do .50mg EOW) and would Love to kiss mandatory donations goodbye! But, it's hard to justify spending $$, putting pharmaceuticals in my body and not getting a quantifiable benefit! i.e. for me personally, it seems if I went low enough on my dosage to eliminate both the AI and Donations, the benefits do not outweigh the cost or the Risks. (IMHO.)
Maybe I'm just damaged goods?

I have ZERO confidence in LTC's protocol, Cypionate, or their Lab's anymore. So, I've got to make a better choice moving fwd. At this point, knowing what I know, I've got no one to blame but myself!

Man, I thank you immensely for all the time and credible effort you put forth on these threads