High Testosterone on only 80mg/week

Buy Lab Tests Online
Also please enlighten us on where you attended medical school and where you got your degree in endocrinology?
Your argument is small-minded and weak. If I told you, the moon revolves around the earth and the earth revolves around the sun, so by your logic, I don’t know what I’m talking about because I didn’t take a course in planetary science or have the proper degree?

That’s a weak argument if I’ve ever heard of one! This attack on my lack of credentials isn’t fooling anyone, this is a deflection or distraction due to your lack of understanding why injecting twice per week is sometimes preferred and recommended.

You don’t have to have attended medical school to be able to read studies and medical journals. We provide the facts as they become available.

You don’t need a medical degree to parrot what you’ve learned from reading studies and medical literature and even listening to well renowned world recognized doctors in this field of medicine.

This is crazy, this all stems from me, recommending more frequent injections than once per week, absolutely insane! I even provided a study recommending twice per week injections and still you have the audacity to challenge it.

If you had done your research like I originally recommended, you would know that when we recommend more frequent injections we always recommend lowering your dose. The smaller peaks and troughs from the smaller more frequent doses can actually relieve side effects of treatment as some people are very sensitive to androgens, having different sensitivity levels at the receptors, receptor density as well as the ability for tissues to respond.

There was a guy a couple of months ago that had prostate cancer and his original testosterone value was under 100 and it took him a while to figure out that he couldn’t handle anything over 300 ng/dL.

Good luck keeping him in a good range for him on once weekly injections!
When you take smaller doses more frequently it is great at first, then the half-lives start to add up.
You’re continuing to embarrass yourself, stop now while it’s not too late!

Actually, wait a minute, maybe it is too late.

These drugs have a half-life of around 7 to 10 days.
Actually, on average is 5 to 7 days.
 
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Defy Medical TRT clinic doctor
As for my advice to the poster, I know personally of two people I have given similar advice to, both had strokes under the age of fifty. One with a hematocrit of 50 and one with a 51!!!!!

https:www.researchgate.net/publication/317572206 Hematocrit and Stroke A Forgotten and Neglected Link.
Lots of diseases or conditions like sleep apnea increase the hematocrit, I have a friend that died a couple of years ago from sleep apnea. It caused, triggered a heart attack in his sleep at 79 years old.

It wasn’t high hematocrit that killed him, it was hypoxia that triggered heart attack! The high hematocrit is always secondary to something else going on.
 
Based on the comments you made here about a hematocrit of below 54 being safe are you willing to stand liable for giving out this false information if the OP has a stroke or heart attack?

Also please enlighten us on where you attended medical school and where you got your degree in endocrinology?

If you are having to give blood to reduce the hematocrit, you are not on "TRT" you are taking a small steroid cycle and calling it TRT.

As for my advice to the poster, I know personally of two people I have given similar advice to, both had strokes under the age of fifty. One with a hematocrit of 50 and one with a 51!!!!!

https:www.researchgate.net/publication/317572206 Hematocrit and Stroke A Forgotten and Neglected Link.

I have personally met Abraham Morgentaler, and greatly respect his work. The endocrinologist that I spoke of in my previous post is greatly respected by Dr. Morgentaler. This person was the main influence on the current guidelines set by the Endocrine Society for TRT.

Dr Morgentaler would be appalled that you use his name to reinforce your ridiculous comments.

First of all, Dr Morgentaler preferred method of treatment is gels! He aims to always maintain a treatment response in the 500 to 600 range! Does not recommend TRT to men with a hematocrit over 50. He would laugh you out of his office if you told him you maintain a total testosterone of 1600!

Please do keep your testosterone over 1000 and use 54 percent hematocrit as a cut off and let us know how this works for you over the years!

You clearly have not done your research!

No one stating here to let your hematocrit run wild!

Again if one has no underlying health issues and is not experiencing any negative sides most in the know specializing in testosterone therapy would not fret if the patient's hematocrit falls within 50-54%.

Yes some will be more cautious and take measures once hematocrit hits 52%.

Most of the endos are sticklers and hesitate once your hematocrit gets over the top end and prefer to keep patients levels no higher than 50%.

LMFAO that would be Bhasin you are referring too.

Well aware of the guidelines let alone the research as I have posted numerous threads over the years!

Let me be clear here when it comes to treating men for low T especially when it comes to TT/FT levels needed in order to not only achieve a healthy FT but more importantly relief/improvement of low-T symptoms and overall well-being Bhasin and Morgentaler are not even on the same page!

Morgentaler is light years ahead of any endo!

The majority of endos are sticklers for numbers/labs over symptom relief whereas Morgentaler is the complete opposite!

Your killing me here with your nonsense!

Caught upon the 2018 Endocrine Society guidelines I see!

Did you even read over the guidelines?

Better yet!






* 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



Screenshot (37150).png

Screenshot (37151).png

Screenshot (37152).png





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%


Screenshot (37153).png

Screenshot (37154).png





Left out those other governing bodies I see!

What do the other governing bodies have to say?

*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

My doctor is one of the top uros in Canada and as stated previously the cutoff is 55% in Canada as per the CUA (Canadian Urological Association) guidelines for Testosterone Therapy

If one has no underlying health issues and is not experiencing any sides he is not too concerned with a hematocrit that falls within 50-55% but tends to recommend donating blood 52-55% or in some cases lowering the T dose and bringing down the FT.

*Canadian guidelines cite 55% as the safe upper limit


*The Endocrine Society uses a hematocrit threshold of >50% as a relative contraindication to initiating TT and >54% as an indication to discontinue treatment [1]. The European Association of Urology (EAU) guidelines on hypogonadism also state that the hematocrit should not exceed 54%, while recent Canadian guidelines cite 55% as the safe upper limit [15, 40]. The AUA guidelines on testosterone deficiency define polycythemia as a hematocrit of 52% and recommend stopping or reducing treatment if the hematocrit reaches 54% [14]







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.
    • If the hematocrit is above 54%:
      • 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.



When Morgentaler was in practice his preference was injections not transdermal as many men have issues with absorption let alone hitting high enough TT/FT levels.

No he is not a stickler for keeping your T levels mid-range!

Pure nonsense.

Watch his numerous interviews/lectures that I posted on the forum.

Yes Morgentaler let alone any doctor that follows the numerous guidelines would recommend against starting TRT if hematocrit is 50%..

Even then Morgentaler was never a stickler for having to keep the hematocrit <50% while on TRT or better yet as he would say Testosterone Therapy (TTh)!




We are talking up do date here is an 20f**KING24 man!

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






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.





 
Based on the comments you made here about a hematocrit of below 54 being safe are you willing to stand liable for giving out this false information if the OP has a stroke or heart attack?

Also please enlighten us on where you attended medical school and where you got your degree in endocrinology?

If you are having to give blood to reduce the hematocrit, you are not on "TRT" you are taking a small steroid cycle and calling it TRT.

As for my advice to the poster, I know personally of two people I have given similar advice to, both had strokes under the age of fifty. One with a hematocrit of 50 and one with a 51!!!!!

https:www.researchgate.net/publication/317572206 Hematocrit and Stroke A Forgotten and Neglected Link.

I have personally met Abraham Morgentaler, and greatly respect his work. The endocrinologist that I spoke of in my previous post is greatly respected by Dr. Morgentaler. This person was the main influence on the current guidelines set by the Endocrine Society for TRT.

Dr Morgentaler would be appalled that you use his name to reinforce your ridiculous comments.

First of all, Dr Morgentaler preferred method of treatment is gels! He aims to always maintain a treatment response in the 500 to 600 range! Does not recommend TRT to men with a hematocrit over 50. He would laugh you out of his office if you told him you maintain a total testosterone of 1600!

Please do keep your testosterone over 1000 and use 54 percent hematocrit as a cut off and let us know how this works for you over the years!

First of all, Dr Morgentaler preferred method of treatment is gels! He aims to always maintain a treatment response in the 500 to 600 range! Does not recommend TRT to men with a hematocrit over 50. He would laugh you out of his office if you told him you maintain a total testosterone of 1600!

Please do keep your testosterone over 1000 and use 54 percent hematocrit as a cut off and let us know how this works for you over the years!
If you are having to give blood to reduce the hematocrit, you are not on "TRT" you are taking a small steroid cycle and calling it TRT.



I'm not 'done with you yet flapping at the gums!

Your stepping on the wrong set of toes with this nonsense.

8 years in and still going strong.

Blood work is stellar and yes I have always run a high-end trough TT/FT.

Those beloved injections (150 mg T) split twice-weekly strictly sub-q.

Yes my hematocrit hovers 50-52% and I feel great overall no sides other than a big, hard vascular dick LMFAO!

Horny, hairy and hard they say!

Guess I'm on a small steroid cycle I can feel the rage!

AARGHHH where's me spinach I mean where's me DIANABOL forgive me I'm turning f**king GREEN!

Screenshot (37168).png



Go push your fear mongering elsewhere you are hitting up the wrong forum!

Better yet take up another hobby!









He is not talking PEAK F**KING levels here!

*Some men feel great at T 400 others notice no benefits until T>700




Therapeutic target levels


*Inadequately studied

*Enormous variation is response from person to person


*Some men feel great at T 400 others notice no benefits until T>700

*Most important question is how are you doing with treatment?


1719100160746.png









Again he is not talking PEAK F**KING levels here!

*Optimal results often require T values in upper range of normal (T 600-900)





*Goal for most patients is symptomatic improvement

*Optimal results often require T values in upper range of normal (T 600-900)

1719100572635.png









Where does Abe stand when treating men for low testosterone.....restoration of ROBUST YOUTHFUL LEVELS!

Key point here being ROBUST!


*Some groups target T levels 1200-1800 ng/dL

*This is a different philosophy of treatment


*Supraphysiological/pharmacological rather than restoration of robust youthful levels

1719100871812.png
 
We could pick this apart too!

When it comes to the half-lifes TE/TC are basically interchangeable.

Numerous threads posted on the forum with some studies thrown in there to boot!

Even then many of the top uros are recommending injecting twice-weekly vs once weekly as the main advantage here is clipping the peak--->trough and blood levels will be more stable throughout the week.

Downfall when injecting once weekly is there will be a big difference in the peak--->trough and blood levels will not be as stable throughout the week especially when injecting strictly IM which a common practice.

This will result in what we call the roller coaster type effect where T levels will be very high at the peak (8-12 hrs) post-injection/during the first 2-3 days every week only to be followed by much lower levels come weeks end which can easily have a negative effect on energy,mood, libido and erectile function.

Top it all off that once weekly injections can have a stronger impact on driving up the hematocrit!
I could site numerous studies that show that doses of more than once weekly drive-up hematocrit levels because of the half-life of the drug adding up. In point of fact studies have shown that weekly doses raise hematocrit more than dosing every two weeks. I won't bother to site the studies as I doubt seriously if you could read them.


As for keeping levels constantly stable this is not how the body works. The body constantly has highs and lows and actually works best when this is duplicated. Why do you think you must get a testosterone test before 8am for it to be accurate? Because it is high in the morning and low at night. However, with all this being said, I would recommend you take hourly doses, keep your total testosterone around 2000ng/dl and consult with the people with no training at all on the internet forums!
 
First of all, Dr Morgentaler preferred method of treatment is gels! He aims to always maintain a treatment response in the 500 to 600 range! Does not recommend TRT to men with a hematocrit over 50. He would laugh you out of his office if you told him you maintain a total testosterone of 1600!

Please do keep your testosterone over 1000 and use 54 percent hematocrit as a cut off and let us know how this works for you over the years!
If you are having to give blood to reduce the hematocrit, you are not on "TRT" you are taking a small steroid cycle and calling it TRT.



I'm not 'done with you yet flapping at the gums!

Your stepping on the wrong set of toes with this nonsense.

8 years in and still going strong.

Blood work is stellar and yes I have always run a high-end trough TT/FT.

Those beloved injections (150 mg T) split twice-weekly strictly sub-q.

Yes my hematocrit hovers 50-52% and I feel great overall no sides other than a big, hard vascular dick LMFAO!

Horny, hairy and hard they say!

Guess I'm on a small steroid cycle I can feel the rage!

AARGHHH where's me spinach I mean where's me DIANABOL forgive me I'm turning f**king GREEN!

View attachment 45557


Go push your fear mongering elsewhere you are hitting up the wrong forum!

Better yet take up another hobby!









He is not talking PEAK F**KING levels here!

*Some men feel great at T 400 others notice no benefits until T>700




Therapeutic target levels


*Inadequately studied

*Enormous variation is response from person to person


*Some men feel great at T 400 others notice no benefits until T>700

*Most important question is how are you doing with treatment?


View attachment 45554








Again he is not talking PEAK F**KING levels here!

*Optimal results often require T values in upper range of normal (T 600-900)





*Goal for most patients is symptomatic improvement

*Optimal results often require T values in upper range of normal (T 600-900)

View attachment 45555








Where does Abe stand when treating men for low testosterone.....restoration of ROBUST YOUTHFUL LEVELS!

Key point here being ROBUST!


*Some groups target T levels 1200-1800 ng/dL

*This is a different philosophy of treatment


*Supraphysiological/pharmacological rather than restoration of robust youthful levels

View attachment 45556
First of all if you were not terribly insecure about your penis size you would not be trying to convince yourself and others on an internet forum that it is even normal. Secondly, I did not know little girls had dicks!!
 
First of all, Dr Morgentaler preferred method of treatment is gels! He aims to always maintain a treatment response in the 500 to 600 range! Does not recommend TRT to men with a hematocrit over 50. He would laugh you out of his office if you told him you maintain a total testosterone of 1600!

Please do keep your testosterone over 1000 and use 54 percent hematocrit as a cut off and let us know how this works for you over the years!
If you are having to give blood to reduce the hematocrit, you are not on "TRT" you are taking a small steroid cycle and calling it TRT.



I'm not 'done with you yet flapping at the gums!

Your stepping on the wrong set of toes with this nonsense.

8 years in and still going strong.

Blood work is stellar and yes I have always run a high-end trough TT/FT.

Those beloved injections (150 mg T) split twice-weekly strictly sub-q.

Yes my hematocrit hovers 50-52% and I feel great overall no sides other than a big, hard vascular dick LMFAO!

Horny, hairy and hard they say!

Guess I'm on a small steroid cycle I can feel the rage!

AARGHHH where's me spinach I mean where's me DIANABOL forgive me I'm turning f**king GREEN!

View attachment 45557


Go push your fear mongering elsewhere you are hitting up the wrong forum!

Better yet take up another hobby!









He is not talking PEAK F**KING levels here!

*Some men feel great at T 400 others notice no benefits until T>700




Therapeutic target levels


*Inadequately studied

*Enormous variation is response from person to person


*Some men feel great at T 400 others notice no benefits until T>700

*Most important question is how are you doing with treatment?


View attachment 45554








Again he is not talking PEAK F**KING levels here!

*Optimal results often require T values in upper range of normal (T 600-900)





*Goal for most patients is symptomatic improvement

*Optimal results often require T values in upper range of normal (T 600-900)

View attachment 45555








Where does Abe stand when treating men for low testosterone.....restoration of ROBUST YOUTHFUL LEVELS!

Key point here being ROBUST!


*Some groups target T levels 1200-1800 ng/dL

*This is a different philosophy of treatment


*Supraphysiological/pharmacological rather than restoration of robust youthful levels

View attachment 45556
I would take double doses of the Dianabol, up the dose of testosterone, eat lots of red meat and saturated fat. Soon, the internet won't be misled by your lack of intelligence
 
BruceWayne, you're acting like an idiot. Notice I'm not saying you're an idiot, simply that you're acting like one. Sure, you can have a difference of opinion with one of our most informed members, but insulting them with derogatory remarks is unacceptable and, in fact, an insult to the integrity of this forum. Members here are dedicated to the intelligent and responsible use of anabolics and while the fine line between that and excessive use sometimes blurs, for the most part discipline is maintained. There is no need to quote the unfortunates who were unable to do so; I'm sure members are as aware of them as you are. My suggestion is to contribute in a positive manner, in an effort to build rather than demolish what has thus far been a well respected discussion site.
 
I could site numerous studies that show that doses of more than once weekly drive-up hematocrit levels because of the half-life of the drug adding up. In point of fact studies have shown that weekly doses raise hematocrit more than dosing every two weeks. I won't bother to site the studies as I doubt seriously if you could read them.


As for keeping levels constantly stable this is not how the body works. The body constantly has highs and lows and actually works best when this is duplicated. Why do you think you must get a testosterone test before 8am for it to be accurate? Because it is high in the morning and low at night. However, with all this being said, I would recommend you take hourly doses, keep your total testosterone around 2000ng/dl and consult with the people with no training at all on the internet forums!

I could site numerous studies that show that doses of more than once weekly drive-up hematocrit levels because of the half-life of the drug adding up. In point of fact studies have shown that weekly doses raise hematocrit more than dosing every two weeks. I won't bother to site the studies as I doubt seriously if you could read them.

LOL post em up!

The site is loaded with studies, lectures, interviews with some of the top-experts in the field and no we are not talking just endos here LMFAO!

Listen closely 34:04-49:36
This is only one of many webinars with some of the top in the field stating how they switch their patients over from once weekly to twice weekly injections in order to clip the peak--->trough let alone maintain more stable/reasonable blood levels throughout the week which will have a big impact on hematocrit.

Still caught up on that peak--->trough LOL!

No one told you it is not just about the peak--->trough/how high you drive up your peak T but more importantly how high you run your FT level at steady-state!

Yes one can inject more frequently using lower weekly doses and easily bring down their FT steady-state let alone clip the peak--->trough which can bring down the hematocrit!

Whether injecting once weekly, twice-weekly, every 3.5 days, 3X weekly, EOD or daily one can easily lower their peak T let alone trough by simply lowering their weekly dose and bringing down their FT peak/steady-state plain and simple!

Big difference in peak--->trough injecting once weekly vs EOD or daily!

No one in the know is prescribing those old outdated piss poor protocols 200 mg T every 2 weeks.

Injecting 200 mg esterified TC/TE every 2 weeks to treat low-t symptoms let alone long-term is a horrible protocol due to the PKs.

Very few men would reap the full beneficial effects of having healthy FT levels on such protocols due to the extreme swing in hormones.

It is a given that you would be back to being hypogonadal before the 2 week mark on such protocol.

You clearly lack the understanding of the PKs/half-lifes and again TE/TC are basically interchangeable!

Better throw this in here too seeing as you are clueless.




Regarding those struggling with high hematocrit here is my reply from another thread:

As you can see your RBCs/hemoglobin/hematocrit is elevated which is a common side-effect when using exogenous T, especially when running higher FT levels let alone peak--->trough levels can have a significant impact.

When using exogenous T RBCs, hemoglobin and hematocrit will increase within the 1st month and can take anywhere from 6-12 months to reach peak levels.

T formulation, the dose of T, genetics (polymorphism of the AR), age all play a role in the impact a trt protocol will have on blood markers (RBCs/hemoglobin/hematocrit).

Other factors such as sleep apnea, smoking, asthma, COPD can have a negative impact on hematocrit.

Injectable T has been shown to have a greater impact on increasing HCT compared to transdermal T.

3–18% with transdermal administration and up to 44% with injection.

In most cases when using injectable T high supra-physiological peaks post-injection and overall T levels (running too high TT/FT level) steady-state will have a big impact on increasing HCT.

Manipulating injection frequency by injecting more frequently using lower doses of T resulting in minimizing the peak--->trough and maintaining more stable levels may lessen the impact on HCT but it is not a given as many men still end up running too high a FT level steady-state!

As again running very high TT/FT levels will have a stronger impact on driving up HCT.

Although injectables have been shown to have a greater impact on HCT you can see even when using a transdermal formulation that maintains stable serum concentrations that the impact it has on HCT is DEPENDANT ON THE DOSE AND SERUM LEVEL OF T.

Using higher doses of transdermal T and achieving higher TT/FT levels will have a greater impact on HCT levels.

How high an FT level you are running is critical.

It is a given that most men on trt struggling with elevated RBCs/hemoglobin/hematocrit are running too high an FT level.

Sure some men are more sensitive than others as they may still struggle with elevated blood markers when running lower T levels but it is far from common and many may already have an underlying health issue contributing to such.

If you are struggling with such blood markers then in most cases finding the lowest FT level you can run while still maintaining the beneficial effects may very well be the solution.

Easier said than done as many men on trt tend to do better running higher-end FT levels within reason.

Mind you some are lucky and never have an issue or levels tend to stabilize over time.

Others will continue to struggle until the cows come home.

Unfortunately too many are caught up in running absurdly high trough FT levels due to the herd mentality spewed on the bro forums and gootube!




As for keeping levels constantly stable this is not how the body works. The body constantly has highs and lows and actually works best when this is duplicated. Why do you think you must get a testosterone test before 8am for it to be accurate? Because it is high in the morning and low at night. However, with all this being said, I would recommend you take hourly doses, keep your total testosterone around 2000ng/dl and consult with the people with no training at all on the internet forums!

No shit sherlock!

Natural endogenous testosterone secretion is pulsatile and diurnal.

During the natural 24-hour circadian rhythm of a healthy young male T levels will start rising gradually overnight reaching a peak (highest point) in the early AM followed by lower levels in the late afternoon and reaching trough (lowest point) in the evening.

Fluctuations from peak--->trough would be around 20-25%

One daily peak/trough.

Many fail to realize that T levels gradually rise overnight reaching a peak in the early AM.

*elevated and near peak TT level during nighttime sleep, peak TT level around the time of morning awakening

*T production occurs in the greatest amount during sleep as recurring pulses at approximately 90 min intervals in healthy young males and approximately 140 min in healthy middle-aged males (91).


This is key:

(i) elevated and near peak TT level during nighttime sleep, (ii) peak TT level around the time of morning awakening, (iii) moderately elevated TT level during the initial hours of wakefulness, (iv) reduced TT level in the late afternoon, and (v) lowest TT level in the evening. Based upon these criteria, only the Androderm® transdermal patch (Figure 3D), when applied in the evening (∼22:00 h) as recommended, closely mimics the TT circadian rhythm of normal young adult males.




*There are substantial differences between the therapies in the derived TT 24 h pattern; moreover, all but one of them differs either somewhat or greatly from the normative one of diurnally active young adult males, which is defined by:

(i) elevated and near peak TT level during nighttime sleep, (ii) peak TT level around the time of morning awakening, (iii) moderately elevated TT level during the initial hours of wakefulness, (iv) reduced TT level in the late afternoon, and (v) lowest TT level in the evening. Based upon these criteria, only the Androderm® transdermal patch (Figure 3D), when applied in the evening (∼22:00 h) as recommended, closely mimics the TT circadian rhythm of normal young adult males.

*The Jatenzo® oral soft gel capsule formulation ingested twice daily at equal intervals also gives rise to variable TT levels of distinct 12 h patterning, with prominent Cmax following 2 to 4 h after each ingestion and rapidly declining levels thereafter (Figure 3B).

*As shown in the graphs of Figures 2 and 3, the PK of most FDA-approved PA-TRTs gives rise to TT 24-hour patterns that deviate greatly from the normative one thereby failing to satisfy one or more of the five specified criteria.


*The temporal patterns of these PA-TRTs differ from normal, either in the timing of the peak and/or nadir TT concentrations, by achieving the highest hormone levels generally between midmorning and noon and lowest (rather than near peak) ones during sleep (Figure 2A-2F).


Hate to burst your bubble here but the closest one would even ever mimic such is using the T patch (Androderm) applied before bed!

It was recently pulled off the market.

Wonder why!

No one would even waste their time using it as many could never even achieve a high enough FT level to derive the full beneficial effects of T let alone there are many other formulations which are far superior in many ways!












However, with all this being said, I would recommend you take hourly doses, keep your total testosterone around 2000ng/dl and consult with the people with no training at all on the internet forums!


You tell em CHAMP!

We have some bright beautiful minds on Excel that are light years ahead of those Endos nutsacks you cling too!
 
@BruceWayne

BruceWayne said:
First of all if you were not terribly insecure about your penis size you would not be trying to convince yourself and others on an internet forum that it is even normal. Secondly, I did not know little girls had dicks!!




First of all if you were not terribly insecure about your penis size you would not be trying to convince yourself and others on an internet forum that it is even normal.


Yeah I was being dead serious LMFAO!

Clearly went over your head!





Secondly, I did not know little girls had dicks!!


Coming from a 66 year old man from Florida.....IMPRESSIVE LOL!

At least I'm not the one that got caught hiding behind the bush playing with ROBIN!
 
Beyond Testosterone Book by Nelson Vergel
I would take double doses of the Dianabol, up the dose of testosterone, eat lots of red meat and saturated fat. Soon, the internet won't be misled by your lack of intelligence

Maybe in my younger wilder years LMFAO!

How did you know I love red meat and those delicious LCFAs?

Bulk mode would be 2 pounds/day, a whopping 500-600 grams complex carbs, those delicious SFAs/MUFAs and a shitload of vegetables!

Blood work is stellar by the way thanks for asking!

I'm in great shape to boot!

Who knew!

Yes I'm also running a high trough TT/FT level using therapeutic doses of T and my hematocrit hovers 50-52% hope I don't drop dead before my birthday its coming up soon!
 
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