The Health Optimization Doctors RoundTable: High Hematocrit Not Important?

[Nelson Vergel]

As I've posted before, having coached people with frailty issues, if higher T/anabolic levels significantly help resolve that issue, the benefits of that alone would likely outweigh any negatives cited here

I agree.

I used 400 mg per week of testosterone plus 200 mg of nandrolone for a while to reverse my wasting syndrome back in the early 90's. Everything in life has to be decided after an internal risk-to-benefit ratio debate.

Built to Survive

Nelson Vergel pushes for the development of new salvage therapies.

www.poz.com

 

[Gianluca]

KEY POINTS FROM EMERGING DATA:

TRT for men with low T levels is good for the heart if the hematocrit is not significantly elevated. (Several studies)

TRT for men with low T using T gels: There is no increased heart risk, but there is an increased incidence of palpitations and arrhythmias for some. (TRAVERSE STUDY)

TRT for men on low T who eventually have long term exposure to hematocrit over 52: There is growing evidence that an unmanaged high hematocrit may not be as great, especially during the first year. (Ramasamy)

Thanks Nelson, that’s a good summary!

 

[tareload]

risk-to-benefit

What risk? Dr.RobRoy tells us there is no risk, just benefits. 1000 to 2000 ng/dl? No problems, you are all good to go.

Get off these forums and listen to TOT Roundtable.

LoL.

E2 Climbing on Same Test Dose + Heartburn

Read a lot tell me how you don’t know what hormone optimization is without telling me you don’t know what hormone optimization is. I understand you with your medical problems and atrial fibrillation from utilizing anabolic steroids do you want men to have optimal testosterone levels. I think...

forums.t-nation.com

Woke TRT. Dude you are too much.

 

[SteveCleves]

Woke TRT. Dude you are too much.

Bro. Your calcium score is zero?????? Fucking woke communist pussy.

 

[aneuman]

Bro. Your calcium score is zero?????? Fucking woke communist pussy.

I guess I am a fucking woke communist pussy too...but guess I always knew that.

 

[SteveCleves]

I guess I am a fucking woke communist pussy too...but guess I always knew that.

View attachment 33716

At the risk of “if you’re explaining the joke it’s not a good joke”. I was making a sarcastic comment on @readalot observation that this ridiculous round table called it “woke TRT” to be conservative with your dosages and to be cautious about the possible cardio side effects of TRT.

 

[aneuman]

At the risk of “if you’re explaining the joke it’s not a good joke”. I was making a sarcastic comment on @readalot observation that this ridiculous round table called it “woke TRT” to be conservative with your dosages and to be cautious about the possible cardio side effects of TRT.

I suspected it (though you never know nowadays) but had to brag anyway. The last portion of my comment was sort of acknowledging your sarcasm…in disguise with plausible deniability, to avoid WW3 in case you were being serious.

there you go, I had to explain mine too… am I being too woke?

 

[Hyrulewarrior1978]

I would be questioning the ethics of any doctor trying to promote the use of a drug to elevate levels of anything outside of the established normal ranges. This is why it’s never a good idea to take advice from physicians who advertise themselves on YouTube and various other social media outlets.

 

[JmarkH]

outside of the established normal ranges.

Therein is the problem. Most of the "ranges" are not well established. AND Therefore the reason for the discussion. Even here on this board, we waffle back and forth over whether the upper measure of TT is really a reasonable upper limit. The waffle, while circling the wagons around the fact the lab companies have set our limit, not the medical experts.

 

[BigTex]

Speaking of testosterone specifically....Labcorp got this ball rolling all because of a single research study. Rather than finding out why norms are shifting Labcorp decided to just lower the bar.

https://www.labcorp.com/assets/11476

Harmonized Reference Ranges for Circulating Testosterone Levels in Men of Four Cohort Studies in the United States and Europe - PubMed

Harmonized normal range in a healthy nonobese population of European and American men, 19 to 39 years, is 264 to 916 ng/dL. A substantial proportion of intercohort variation in testosterone levels is due to assay differences. These data demonstrate the feasibility of generating harmonized...

pubmed.ncbi.nlm.nih.gov

 

[Guided_by_Voices]

I would be questioning the ethics of any doctor trying to promote the use of a drug to elevate levels of anything outside of the established normal ranges. This is why it’s never a good idea to take advice from physicians who advertise themselves on YouTube and various other social media outlets.

"normal ranges" in the US are based on a sick, unhealthy population. I would question the competence and ethics any doctor that relied on "normal" ranges for anything. This is especially true for a patient who has "catching up" to do.

 

[BigTex]

Exactly why some doctors are treating symptoms and not numbers

BMI Categories:
Underweight = <18.5
Normal weight = 18.5–24.9
Overweight = 25–29.9
Obesity = BMI of 30 or greater

So LabCorp believes that healthy is being over weight? But seems the AMA disagrees with the BMI being used at all because of its racial bias.

BMI standards are ‘racist’: American Medical Association

The largest organization of doctors in the U.S., is ready to say “goodbye” to determining healthy body weight solely by BMI.

nypost.com

 

[RobRoy]

This study was done with T gels and max hematocrit was 52

View attachment 33680

When you take the time to actually read the study and the details you'll see that 52% was just the highest that they got. If you would've gone higher than that they would've used a different number but that's the highest hematocrit they got on the dose. They didn't stop there it's just as high as it went in those men on that specific dose. If it would have gone up to 54 or 55 you would've seen the same thing. You heard multiple experts at the androgen society state that there is no harm with increasing hematocrit and that included Morgentaler.

 

[RobRoy]

I am showing some interesting patient withdrawal and dropout data here (post #10)

Effects of Long-term Testosterone Treatment on Cardiovascular Outcomes in Men with Hypogonadism

ABSTRACT Background: Testosterone exerts some effects on the cardiovascular system that could be considered beneficial; some other effects may potentially increase the risk of cardiovascular (CV) events. Neither the long-term efficacy nor safety of testosterone treatment has been studied in an...

www.excelmale.com

Reason that is what we've been saying for the years and what is become a problem on this website which is the woke TRT movement. When you only give me an a little bit and then the study they only raised it to 750 or less than most men are not gonna do any better and they're going to drop out. If you wanna double that there wouldn't be much of a drop out. But there was basically as much drop out in the placebo as the treatment arm. Raise testosterone a little bit and men will only do a little bit better or no better at all

 

[RobRoy]

Look....I even save time for @RobRoy

Does Estrogen Make Me Fat? What about Fertility?

Hey Tareload, I spoke specifically with the author of this article in Florida just two months ago. I had a very specific conversation with doctor Ramasamy after he presented this article. Guess what? His statement was that he doesn’t feel the increase in hematocrit is harmful on testosterone...

forums.t-nation.com

That makes me the Dummy to continue interacting with someone who won't operate in good faith. Nice chatting again @RobRoy . Can't wait for your next video. Make sure to issue me a public apology. And get Scott on there too.

Benefits of Estrogen for TRT Patients

@readalot I wasn’t going to let you down. Here it is from the smartest man I know. There is some semblance of a chain of reasoning but several aspects are ignored. What does viscosity mean to healthy men without hematological disorders? Do the kinetics of the blood favor developing conditions...

forums.t-nation.com

You Don't even realize that what you posted isn't a study do you? We discussed Ramasamy in the video if you would take the time to listen and if you did you would actually learn something. That was a retrospective data mining study. Just like the vigan and finkel studies. Absolutely worthless and that's why you haven't had this paper get any traction because it was recognized immediately as a retrospective data mining study which cannot do anything with regard to establishing causation. Discussed at the androgen Society meeting and it was pooh-poohed because of exactly what I said it was a data mining retrospective worthless study. But you keep using it to propagate your faults negative because you have nothing else. They are interesting and thought provoking but that's about it. And yet you have a study that comes out that was actually a prospective study around the same time that showed a level of 52% as being protective. The only reason 52% was used was because that's the highest level of hematocrit they got in the study on that particular dose.
We need to be cautious regarding the information derived from weak retrospective database studies.


In 2013 and 2014 two retrospective database studies were published that got a lot of media exposure because of their findings of increased cardiovascular events in men


The first was the Vigen Study that used a national veterans administration prescription database and the other was by Finkle who used an insurance claims database.


These studies were subsequently exposed as being extremely flawed with major limitations





The most recent study by Ory et al (Ramasamy) suggesting an increase in major adverse cardiac events in men secondary to an increase in hematocrit was also a retrospective database study based on electronic medical records.





Understand that all of these studies are retrospective studies and not a planned experiment so conclusions must be regarded extremely cautiously as these types of studies are prone to error and bias.


They have an inferior level of evidence compared with prospective studies


They are subject to confounding as other risk factors that may have been present or not measured


And most importantly retrospective studies cannot determine causation they can only show an association.


They are thought-provoking and hypothesis generating but findings have to be proven by larger more expensive prospective studies.





A recent prospective study my Strange et al showed that an increase in hematocrit of up to 52% with testosterone therapy is associated with decrease mortality. The only reason they cut it off at 52% was that no one exceeded that in their study.





So it appears that when someone wants to do a study that shows increased risk with testosterone then they always resort to a weak retrospective database study and what's most concerning is that many of these studies appear to be a data mining exercise with the express goal of obtaining a statistically significant result worthy of publication.


In terms of CV risks associated with T-induced erythrocytosis, prospective, randomized, controlled trials have failed to detect a direct relationship between T-induced erythrocytosis and subsequent risk for CV events (including stroke and deep vein thrombosis).Khera





There are no randomized or prospective studies that have documented a direct relationship between testosterone related erythrocytosis and thromboembolic events

 

[RobRoy]

From Ramasamy' study:

View attachment 33684


We demonstrated that developing secondary polycythemia while receiving TT, defined as a hematocrit over 52%, was associated with increased risk of developing MACE and VTE during the first year of therapy. TT itself, in the absence of polycythemia, did not appear to increase risk of MACE/VTE in hypogonadal men. To our knowledge, this is the first study to establish secondary polycythemia from TT as an independent risk factor for MACE/VTE using a specific hematocrit-based cutoff.

We used a large national database to answer this question, hypothesizing that real-world data would be best suited to address this issue. Men with high baseline hematocrit are often excluded from randomized trials, and in clinical practice pre-treatment blood work is often not done, and guidelines are frequently not followed.20,21 This leaves a large population of men using TT who are not represented by RCTs. Our findings are somewhat supported by prior literature.

The TOM (Testosterone in Older Men with Sarcopenia) trial, an RCT that was stopped early due to increased risk of cardiovascular adverse events, included older men with a high incidence of comorbid conditions.22 While this trial only included 209 men, their demographic information is similar in nature to our study, which included a large proportion of men with comorbid conditions. Like most RCTs on testosterone, the TOM trial did not report hematocrit values in those men with cardiovascular events. One systematic review on this topic did not find overall increased cardiovascular risk, however they did find an increased event rate in the first 12 months of therapy, supporting our window of 1 year for evaluation of MACE/VTE.23

Another review reinforced the value of using large databases in answering this question, highlighting that all published RCTs on this topic are underpowered to assess any association with treatment and cardiovascular outcomes.24

This will hopefully be addressed by the TRAVERSE (Testosterone Replacement Therapy for Assessment of Long-term Vascular Events and Efficacy ResponSE in Hypogonadal Men) trial (NCT03518034), however polycythemia or hematocrit-based adverse events are not listed as an outcome.It is well established that TT increases the risk of secondary polycythemia,25 with higher rates in longer-acting modalities and lower rates in shorter-acting modalities.16 Multiple national guidelines use elevation in hematocrit as a trigger to stop or change TT in men.

TT cessation triggers include 55% from Canadian guidelines,9 54% from endocrine society guidelines and European urology guidelines,5,26 and between 50%–54% from American urological guidelines.10 While the rationale for these cutoffs is not cited in these guidelines, they appear to come from the Framingham heart study, which found an increase in adverse cardiovascular outcomes with a hematocrit of 49% or higher.8 These findings were confirmed in a more recent prospective cohort study, which found an increased rate of overall and cardiovascular-related mortality once hematocrit entered the range of 50%–54%.27 Neither of these studies specifically studied men on testosterone, and thus the currently existing hematocrit cutoffs amongst TT users is arbitrary. For the purposes of our study, we chose a cutoff of 52%, reflecting other published literature, and to ensure a relatively large comparator arm.10,16

The strengths of this study include its use of a large multi-institutional database and being a real-world snapshot of the effects of TT in a U.S. cohort. There is increasing evidence that nonrandomized evidence from large databases can accurately emulate a large-scale RCT, lending validity to these results.28 Detailed propensity-score matching increased the validity of our findings. Lastly, our sensitivity analyses, and analysis of TT-naïve men, support the role of polycythemia as an independent, critical factor in the development of MACE/VTE.

Limitations include the inability to segregate results by type of testosterone prescription. In addition, a large percentage of the men included are Caucasian (86%), and the matched populations have a relatively high comorbidity index, limiting the generalizability of the findings to minorities and healthy individuals. Furthermore, we were not able to match the 2 groups by baseline hematocrit, as the men in the polycythemia group had a higher baseline hematocrit.
Therefore, we cannot definitively determine whether the increased risk of MACE/VTE is due to hematocrit reaching 52% or due to men with higher baseline hematocrit starting TT. Regardless, the baseline hematocrit in the polycythemia group was 47.4%, which according to U.S., Canadian and European guidelines does not warrant further investigation before starting TT.

Lastly, due to the limitations of the TriNetX database, we were unable to analyze hematocrit as a continuous variable.Regardless of these limitations, this study lends prescribers a practical approach to informing about risks of TT, and reinforces existing guideline practices of checking hematocrit prior to prescribing.5 It also provides a hematocrit-based cutoff that comes directly from a population of men using TT, and can hopefully allow future guideline statements to remain consistent across recommendations. Future studies that aim to assess cardiovascular outcomes in men on testosterone (such as the ongoing TRAVERSE study, NCT03518034) should perform detailed analysis on hematocrit change to investigate this as a possible association.

CONCLUSION​

Men using TT should be aware that they are at a higher risk for MACE/VTE if their hematocrit reaches or exceeds 52% during the first year of therapy. This is especially relevant in men with cardiovascular comorbidities. Hematocrit-based cutoffs should be incorporated into the outcomes of future RCTs investigating MACE/VTE and TT

I know you were at the Androgen Society meeting but you must've been in the restroom or getting some coffee when this retrospective data mining study was discussed. It's not worth the paper it's written on. These retrospective studies cannot determine causation they can at most suggest an association. I discussed the paper with the author himself the year before last and he himself doesn't feel there's any harm in racing hematocrit with testosterone. His particular focus now is on the magnitude of change and hematocrit when somebody starts testosterones not the actual increase in hematocrit absolutely. This study is no different than the vigen and finked studies. Not worth the paper they are written on
We need to be cautious regarding the information derived from weak retrospective database studies.


In 2013 and 2014 two retrospective database studies were published that got a lot of media exposure because of their findings of increased cardiovascular events in men


The first was the Vigen Study that used a national veterans administration prescription database and the other was by Finkle who used an insurance claims database.


These studies were subsequently exposed as being extremely flawed with major limitations





The most recent study by Ory et al (Ramasamy) suggesting an increase in major adverse cardiac events in men secondary to an increase in hematocrit was also a retrospective database study based on electronic medical records.





Understand that all of these studies are retrospective studies and not a planned experiment so conclusions must be regarded extremely cautiously as these types of studies are prone to error and bias.


They have an inferior level of evidence compared with prospective studies


They are subject to confounding as other risk factors that may have been present or not measured


And most importantly retrospective studies cannot determine causation they can only show an association.


They are thought-provoking and hypothesis generating but findings have to be proven by larger more expensive prospective studies.





A recent prospective study my Strange et al showed that an increase in hematocrit of up to 52% with testosterone therapy is associated with decrease mortality. The only reason they cut it off at 52% was that no one exceeded that in their study.





So it appears that when someone wants to do a study that shows increased risk with testosterone then they always resort to a weak retrospective database study and what's most concerning is that many of these studies appear to be a data mining exercise with the express goal of obtaining a statistically significant result worthy of publication.


In terms of CV risks associated with T-induced erythrocytosis, prospective, randomized, controlled trials have failed to detect a direct relationship between T-induced erythrocytosis and subsequent risk for CV events (including stroke and deep vein thrombosis).Khera





There are no randomized or prospective studies that have documented a direct relationship between testosterone related erythrocytosis and thromboembolic events

you actually at the Anderson Society meeting

 

[Keepfit1]

The TRAVERSE study they mentioned was presented recently. However, it only included men on Androgel, not injections. High hematocrit was not as common, so it is a moot subject for most men on this forum on T injections running high T blood levels and hematocrit over 52.

See post 9 above.

I asked my Haematologist once if he sees many for secondry polycythaemia and he said only on injections not gel, to balance that out though its quite hard to get T up high enough 24/7 on Gel, creams maybe/probably

 

[RobRoy]

Shall I post you a pdf of the TRAVERSE study or is that a flawed study? Or did they not get those TT/FT levels high enough? Yeah they got those guys up to sissy levels, I know.

Woke TRT? You just keep getting funnier. Thank you for the entertainment. Call Dr. Scott and read him the study as a bedtime story. LoL.

Lemme guess, that AFIB finding and arythmmia is bullshit as well? Ignore symphathic modulation much, do you?

They even took out the dudes with over 54% Hct from the treatment arm haha.

I watched the whole video BTW. Keep waving your hands or try being intellectually honest for a refreshing change.

Get Danny Bossa over here as well and you can all apologize to me. He had an excuse being a civilian entertainer... What is your excuse?

You can appeal to authority all you want good Doctor and I am glad @Nelson Vergel was there at the meeting with you. You and your circle have lots to discuss now. Can't wait to hear your plans for TRAVERSE II with two treatment arms (20 to 30 ng/dl FT vs 30 to 40 ng/dl FT vs placebo). That's going to be a lot of cream. What do you think will happen? Make sure you don't remove the guys running over 54% Hct as well (just more oxygen in the blood, righr?).

Your lack of clinical experience shows every time you write something. You have no medical training and it shows every time you write something. You might be able to impress the little boys on forums but no one else. Like I've said before you might be some teenage boy living in Indonesia somewhere because no one knows who you are so one of you identify yourself and tell us about all of your medical training and your clinical experience dealing with hormones.
But to specifically address your question. If you notice in the trial it was basically a 50% drop out in both the placebo and the treatment arm. If they were to raise testosterone levels to optimal levels you would've seen that drop out. The maximum level was 750. Wow that's awesome. Everybody feels better with a level of 750 – – – not!. The Afib was that clinically significant? and was the study powered for that? You don't see anybody focusing on that in the national media even do you? Once again it raised a question but we can't ignore decades of other studies that show that testosterone decreases the instances of a fib because it shortens the QT interval. Once again read a lot to those that are in the know you absolutely reveal that you don't know what you don't know.

 

[Systemlord]

When you take the time to actually read the study and the details you'll see that 52% was just the highest that they got.

Raise testosterone a little bit and men will only do a little bit better or no better at all

Those men basically had sissy T levels and I wouldn’t be surprised to see the next randomized placebo controlled trial showing a more positive outcome.

 

[RobRoy]

Look....I even save time for @RobRoy

Does Estrogen Make Me Fat? What about Fertility?

Hey Tareload, I spoke specifically with the author of this article in Florida just two months ago. I had a very specific conversation with doctor Ramasamy after he presented this article. Guess what? His statement was that he doesn’t feel the increase in hematocrit is harmful on testosterone...

forums.t-nation.com

That makes me the Dummy to continue interacting with someone who won't operate in good faith. Nice chatting again @RobRoy . Can't wait for your next video. Make sure to issue me a public apology. And get Scott on there too.

Benefits of Estrogen for TRT Patients

@readalot I wasn’t going to let you down. Here it is from the smartest man I know. There is some semblance of a chain of reasoning but several aspects are ignored. What does viscosity mean to healthy men without hematological disorders? Do the kinetics of the blood favor developing conditions...

forums.t-nation.com

Lets just ignore all the previous studies shall we read a lot?