Nandrolone Experiences

[tareload]

Does Nandrolone increase total testosterone. For instance, if at 100mg/week T Cypionate my total T is 1,000 ngdL and I add 50mg/week Nandrolone will my total T increase above 1,000 ngdL?

If you use LCMS, no.

If you use immunoassay, yes (interference).

Does nandrolone increase total testosterone? NO.

Will it interfere with immunoassay result? yes to some degree depending on instrument.

Nelson basically gives away the LCMS/ED TT/FT tests on DiscountedLabs.com via Quest.

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[Nelson Vergel]

Does Nandrolone increase total testosterone. For instance, if at 100mg/week T Cypionate my total T is 1,000 ngdL and I add 50mg/week Nandrolone will my total T increase above 1,000

It can falsely show as higher testosterone if you use the immunoassay based testosterone test but not if you use the LC/MS test for total testosterone.

 

[Jake_from_StateFarm]

LabCorp uses immunoassay so that will be a problem with my Uro's results.

If I stop the 50 mg/week Nandrolone for a month before my labs, will that give enough time to normalize the panel? I know the ester is long lasting.

 

[tareload]

LabCorp uses immunoassay so that will be a problem with my Uro's results.

If I stop the 50 mg/week Nandrolone for a month before my labs, will that give enough time to normalize the panel? I know the ester is long lasting.

You can also get the LCMS/ED panels from Labcorp.

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

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

www.labcorp.com

 

[Deleted member 43589]

LabCorp uses immunoassay so that will be a problem with my Uro's results.

If I stop the 50 mg/week Nandrolone for a month before my labs, will that give enough time to normalize the panel? I know the ester is long lasting.

Nandrolone Decanoate has an absorption half life of 6 days and an elimination half life of 4.3 hours. Studies have shown that nandrolone decanoate has a terminal half life of 7.1, 11.7, and 11.8 hours for doses of 50, 100, and 150 mg respectively. I have seen guys test positive (urine) in sport up to 12-18 months post injection depending on your body fat levels. For any good or bad this drug may do you always have to remember it is very long acting any any problems will take a while to correct.

Pharmacokinetic evaluation of three different intramuscular doses of nandrolone decanoate: analysis of serum and urine samples in healthy men - PubMed

The pharmacokinetics of nandrolone in serum and urine were investigated in healthy young men after a single im injection of 50 mg (n = 20), 100 mg (n = 17), or 150 mg (n = 17) nandrolone decanoate. Blood samples were collected before treatment and for up to 32 d after dosing. In addition, in the...

pubmed.ncbi.nlm.nih.gov

 

[Steve78]

Long thread. What’s the consensus on say 100 mg weekly for half the year? Will it hinder health and longevity?

 

[Gman86]

Long thread. What’s the consensus on say 100 mg weekly for half the year? Will it hinder health and longevity?

Think it’s unfortunately opinion at this point, due to lack of quality studies/ info on the subject

I personally think using 100mg of nandrolone indefinitely is ok, as long as u are strict with ur diet and lifestyle. I personally use that dose, and have for a few years now. And currently plan on using it indefinitely. So as long as ur on top of
ur diet, exercise regimen, sleep and other lifestyle factors, I personally wouldn’t been too worried about using 100mg of nandrolone for 6 months of the year. @Vince reported that the percentage of his small dense ldl increased while on nandrolone, so that’s something to think about. Not saying that will happen to everyone, but if it happened to him, obv there’s a chance it could happen to others

 

[Jake_from_StateFarm]

I find Taeian Clark's theory of Nandrolone only for six weeks on and five weeks off interesting in that he says androgen receptor down regulation begins after week six. Then take off five weeks and repeat. He also recommends occasionally bumping TRT. For example, bump 100mg/wk to 125mg or 150mg for six weeks and then return to 100mg/wk.

Taeian Clark - Health And Fitness Coach on Instagram: "Androgen receptor down-regulation and its effects on muscle growth. Short vs Long Cycles. Short cycles, supplements to improve androgen receptor content, why androgen receptor content matters fo

65 likes, 10 comments - taeianclark on July 2, 2020: "Androgen receptor down-regulation and its effects on muscle growth. Short vs Long Cycles. Short cycles, supplements to improve androgen receptor content, why androgen receptor content matters for muscle growth, why gains stop by week 6...

www.instagram.com

 

[Deleted member 43589]

I find Taeian Clark's theory of Nandrolone only for six weeks on and five weeks off interesting in that he says androgen receptor down regulation begins after week six. Then take off five weeks and repeat. He also recommends occasionally bumping TRT. For example, bump 100mg/wk to 125mg or 150mg for six weeks and then return to 100mg/wk.

Taeian Clark - Health And Fitness Coach on Instagram: "Androgen receptor down-regulation and its effects on muscle growth. Short vs Long Cycles. Short cycles, supplements to improve androgen receptor content, why androgen receptor content matters fo

65 likes, 10 comments - taeianclark on July 2, 2020: "Androgen receptor down-regulation and its effects on muscle growth. Short vs Long Cycles. Short cycles, supplements to improve androgen receptor content, why androgen receptor content matters for muscle growth, why gains stop by week 6...

www.instagram.com

I have my doubts about androgen receptor shut down.

Bamman MM, Shipp JR, Jiang J, Gower BA, Hunter GR, Goodman A, McLafferty CL Jr, Urban RJ. Mechanical load increases muscle IGF-I and androgen receptor mRNA concentrations in humans. Am J Physiol Endocrinol Metab. 2001 Mar;280(3):E383-90.

Full study
http://ajpendo.physiology.org/content/a ... 3.full.pdf

Abstract
The mechanism(s) of load-induced muscle hypertrophy is as yet unclear, but increasing evidence suggests a role for locally expressed insulin-like growth factor I (IGF-I). We investigated the effects of concentric (CON) vs. eccentric (ECC) loading on muscle IGF-I mRNA concentration. We hypothesized a greater IGF-I response after ECC compared with CON. Ten healthy subjects (24.4 +/- 0.7 yr, 174.5 +/- 2.6 cm, 70.9 +/- 4.3 kg) completed eight sets of eight CON or ECC squats separated by 6-10 days. IGF-I, IGF binding protein-4 (IGFBP-4), and androgen receptor (AR) mRNA concentrations were determined in vastus lateralis muscle by RT-PCR before and 48 h after ECC and CON. Serum total testosterone (TT) and IGF-I were measured serially across 48 h, and serum creatine kinase activity (CK), isometric maximum voluntary contraction (MVC), and soreness were determined at 48 h. IGF-I mRNA concentration increased 62% and IGFBP-4 mRNA concentration decreased 57% after ECC (P < 0.05). Changes after CON were similar but not significant (P = 0.06-0.12). AR mRNA concentration increased (P < 0.05) after ECC (63%) and CON (102%). Serum TT and IGF-I showed little change. MVC fell 10% and CK rose 183% after ECC (P < 0.05). Perceived soreness was higher (P < 0.01) after ECC compared with CON. Results indicate that a single bout of mechanical loading in humans alters activity of the muscle IGF-I system, and the enhanced response to ECC suggests that IGF-I may somehow modulate tissue regeneration after mechanical damage.


DISCUSSION FROM FULL STUDY
We report for the first time changes in muscle mRNAs associated with tissue growth and repair after a single bout of resistance exercise in humans. The novel approach of studying high-intensity CON and ECC loading separately enabled us to test the influence of ECC action on the IGF-I and AR responses to mechanical load. The results indicate that high-intensity lengthening and shortening contractions both induce muscle IGF-I and AR gene transcription. Moreover, the enhanced IGF-I activation after ECC loading supports the concept that IGF-I is somehow involved in tissue regeneration after mechanical load-induced damage.

Kind of blows the theory of desensitization and shut down of AR and IGF-1R doesn't it? However, while exercise increase AR and their sensitivity, there is still probably a saturation point where the more you use the greater the side effects and the less the benefits. This is the same concept with peptides. We know through research that 1mcg/kg/bw is saturation level. The higher you go up past saturation levels the less the benefits and the greater the unwanted side effects.

In other words....enhanced activation of satellite cells by testosterone requires IGF-1. Those Androgens that aromatize are effective at not only increasing IGF-1 levels but also the sensitivity of satellite cells to growth factors. This action has no direct effect on protein synthesis, but it does lead to a greater capacity for protein synthesis by increasing fusion of satellite cells to existing fibers. This increases the number of myonuclei and therefore the capacity of the cell to produce proteins. That is why most likely why large bodybuilders will benefit significantly more from high levels of Androgens compared to a relatively new user.

So whenever a muscle grows in response to training there is a coordinated increase in the number of myonuclei and the increase in fiber cross sectional area. More myonuclei mean more receptors. The same is most likely true for IGF-1 use. The more mechanical loading during training the more muscle damage, the greater hypertrophy. WIth hypertrophy come more myonuclei/satellite cells thus, more AR. So now we have a greater need for IGF-1. So while there is most likely a saturation level for using IGF-1 Lr3, there is absolutely no evidence that IGF-1R shut down or desensitize after 4 weeks of continual use or longer.

 

[Deleted member 43589]

Sinha-Hikim I, Taylor WE, Gonzalez-Cadavid NF, Zheng W, Bhasin S. Androgen receptor in human skeletal muscle and cultured muscle satellite cells: up-regulation by androgen treatment. J Clin Endocrinol Metab. 2004 Oct;89(10):5245-55.
Full Study

Androgen Receptor in Human Skeletal Muscle and Cultured Muscle Satellite Cells: Up-Regulation by Androgen Treatment

Abstract. Androgens stimulate myogenesis, but we do not know what cell types within human skeletal muscle express the androgen receptor (AR) protein and ar

academic.oup.com

Abstract
Androgens stimulate myogenesis, but we do not know what cell types within human skeletal muscle express the androgen receptor (AR) protein and are the target of androgen action. Because testosterone promotes the commitment of pluripotent, mesenchymal cells into myogenic lineage, we hypothesized that AR would be expressed in mesenchymal precursor cells in the skeletal muscle. AR expression was evaluated by immunohistochemical staining, confocal immunofluorescence, and immunoelectron microscopy in sections of vastus lateralis from healthy men before and after treatment with a supraphysiological dose of testosterone enanthate. Satellite cell cultures from human skeletal muscle were also tested for AR expression. AR protein was expressed predominantly in satellite cells, identified by their location outside sarcolemma and inside basal lamina, and by CD34 and C-met staining. Many myonuclei in muscle fibers also demonstrated AR immunostaining. Additionally, CD34+ stem cells in the interstitium, fibroblasts, and mast cells expressed AR immunoreactivity. AR expression was also observed in vascular endothelial and smooth muscle cells. Immunoelectron microscopy revealed aggregation of immunogold particles in nucleoli of satellite cells and myonuclei; testosterone treatment increased nucleolar AR density. In enriched cultures of human satellite cells, more than 95% of cells stained for CD34 and C-met, confirming their identity as satellite cells, and expressed AR protein. AR mRNA and protein expression in satellite cell cultures was confirmed by RT-PCR, reverse transcription and real-time PCR, sequencing of RT-PCR product, and Western blot analysis. Incubation of satellite cell cultures with supraphysiological testosterone and dihydrotestosterone concentrations (100 nm testosterone and 30 nm dihydrotestosterone) modestly increased AR protein levels. We conclude that AR is expressed in several cell types in human skeletal muscle, including satellite cells, fibroblasts, CD34+ precursor cells, vascular endothelial, smooth muscle cells, and mast cells. Satellite cells are the predominant site of AR expression. These observations support the hypothesis that androgens increase muscle mass in part by acting on several cell types to regulate the differentiation of mesenchymal precursor cells in the skeletal muscle.

DISCUSSION FROM FULL STUDY
In summary, although multiple cell types within the human skeletal muscle express AR protein, satellite cells, and myonuclei are the predominant sites of AR expression. ARs aggregate within the nucleoli of satellite cells and myonuclei. Testosterone and DHT up-regulate AR expression in vivo and in vitro. These data are consistent with the proposal that androgens induce skeletal muscle hypertrophy by acting at multiple sites within the muscle through multiple mechanisms, including modulation of pluripotent stem cell commitment and differentiation and regulation of muscle protein synthesis; further studies are needed to elucidate the molecular basis of androgen action on human skeletal muscle.

So when you build muscle using testosterone or other AAS obviously muscle is enlarged and new satellite cells are made therefore AR's are increased in numbers and existing AR are upregulated.


Here is a much more simplified article that explains the same thing,

Androgen Receptor Regulation

One of the most common beliefs concerning anabolic-androgenic steroid (AAS) usage is that the androgen receptor (AR) downregulates as a result of such

thinksteroids.com

 

[Gman86]

I find Taeian Clark's theory of Nandrolone only for six weeks on and five weeks off interesting in that he says androgen receptor down regulation begins after week six. Then take off five weeks and repeat. He also recommends occasionally bumping TRT. For example, bump 100mg/wk to 125mg or 150mg for six weeks and then return to 100mg/wk.

Taeian Clark - Health And Fitness Coach on Instagram: "Androgen receptor down-regulation and its effects on muscle growth. Short vs Long Cycles. Short cycles, supplements to improve androgen receptor content, why androgen receptor content matters fo

65 likes, 10 comments - taeianclark on July 2, 2020: "Androgen receptor down-regulation and its effects on muscle growth. Short vs Long Cycles. Short cycles, supplements to improve androgen receptor content, why androgen receptor content matters for muscle growth, why gains stop by week 6...

www.instagram.com

Ya he’s all about very short cycles, take the equal time off, and hop back on. He says like 90% of the gains in a cycle come within the first 4-6 weeks, or something like that

 

[Steve78]

Ya he’s all about very short cycles, take the equal time off, and hop back on. He says like 90% of the gains in a cycle come within the first 4-6 weeks, or something

For me, I don’t see deca kick in until week 7-8

 

[Gman86]

For me, I don’t see deca kick in until week 7-8

Ya not saying I agree with him at all about this topic Lol. I personally see tiny improvements in muscle every week, and I take the opposite approach as him. I’m more about staying on the same protocol, and seeing very slow and steady gains over the long haul, no cycling. But like I said, I see small improvements in muscle mass every week, so if receptor downregulation is a thing, it doesn’t seem to be effecting me in any way that bothers me. He could be right tho, and as far as gaining lean muscle mass goes, very short cycles, with the same time off, then repeat, might be a better balance of gains and health/ longevity. Just the complete opposite of my style personally

 

[Guided_by_Voices]

I think a key and underappreciated piece of context for discussions like this is whether or not someone is already on TRT. Approaches for microdosing anabolics without creating a problematic degree of T suppression have been completely overshadows by the "always use T" crowd, however I have been hearing more and more influencers mentioning intermittent micro-dosing so perhaps it will make a comeback.

 

[Sly]

Ya not saying I agree with him at all about this topic Lol. I personally see tiny improvements in muscle every week, and I take the opposite approach as him. I’m more about staying on the same protocol, and seeing very slow and steady gains over the long haul, no cycling. But like I said, I see small improvements in muscle mass every week, so if receptor downregulation is a thing, it doesn’t seem to be effecting me in any way that bothers me. He could be right tho, and as far as gaining lean muscle mass goes, very short cycles, with the same time off, then repeat, might be a better balance of gains and health/ longevity. Just the complete opposite of my style personally

My approach is the same as yours.

 

[Jake_from_StateFarm]

Nelson - Am I mistaken or was there a study regarding the prostate benefits associated with occasionally pulsing testosterone above baseline TRT dosage?

 

[Guided_by_Voices]

Nelson - Am I mistaken or was there a study regarding the prostate benefits associated with occasionally pulsing testosterone above baseline TRT dosage?

You're likely thinking of the below, however it's not clear (I have wondered too) if this would be a prudent preventative measure or if it just helps in people who already have PCa. I would think, in the absence of better data, that a high-pulse of T every 6 month would be prudent, but it's unclear.

Prostate Cancer: Bipolar Androgen Therapy (BAT)

Summary Prostate Cancer Lab #56 focuses on Bipolar Androgen Therapy (BAT) as a potential treatment for castration-resistant prostate cancer. The therapy involves alternating between high-dose testosterone injections and the continuation of testosterone-suppressing drugs. BAT has shown positive...

www.excelmale.com

 

[madman]

Nelson - Am I mistaken or was there a study regarding the prostate benefits associated with occasionally pulsing testosterone above baseline TRT dosage?

Having healthy testosterone levels has a protective effect on the health of the prostate.

This can be achieved using therapeutic doses of T for men diagnosed with hypogonadism.

I would be far more concerned with having low testosterone levels long-term!

Pushing TRT dose well beyond therapeutic (400-600 mg/week) serves no purpose other than the sole fact of gaining muscle/strength well beyond ones natural genetic potential.

TRT and the Prostate

Testosterone Treatment and the Risk of Prostate Adverse Events (2022) Jason A. Levy, DO, MS, Arthur L. Burnett, MD, MBA, Adrian S. Dobs, MD, MHS INTRODUCTION Definition Hypogonadism is a clinical syndrome that results from failure of the testis to produce physiologic concentrations of...

www.excelmale.com

Impact of Low Free Testosterone on Prostate Cancer

www.excelmale.com

Low Testosterone in Men: Recommendations on the diagnosis, treatment and monitoring

ABSTRACT The relative proportional increase of the elderly population within many countries will become one of the most significant social transformations of the twenty-first century and, for the first time in history, persons aged 65 or above outnumbered children under five years of age...

www.excelmale.com

BPH/LUTS

*There is no evidence that TTh either increases the risk of BPH or contributes to the worsening of LUTS

*At present, there is no evidence that TTh either increases the risk of BPH or contributes to the worsening of LUTS




PCa

*There is no evidence of increased PCa risk in men on TTh

*Recent evidence fails to support the longstanding fear that T therapy will increase prostate cancer risk or cause rapid growth of occult cancer

*The relationship between testosterone and prostate cancer appears to follow a saturation curve, present in many biological systems, in which growth corresponds with a concentration of a key nutrient until a concentration is reached in which an excess of the nutrient is achieved (Figure 2). Clinical data indicate the saturation point for serum T is approximately 250 ng/dL (8.68 nmol/L)

*There is no evidence that TTh will convert sub-clinical prostatic lesions to clinically detectable PCa

*Nonetheless, in the absence of large-scale, long-term controlled studies, it is impossible to definitively assert the safety of TTh with regard to PCa.

*Therefore, prior to starting TTh, a patient’s risk of PCa must be assessed using, at a minimum measurement of serum prostate-specific antigen (PSA). Pretreatment assessment should include PCa risk predictors such as age, family history of PCa, and ethnicity/race. If suspicion of PCa exists, it may be reasonable to perform a prostate biopsy if warranted by clinical presentation. Testosterone therapy may be initiated in these men if a prostate biopsy is negative

*After initiation of TTh, patients should be monitored for prostate disease with measurement of serum PSA at 3–6 months, 12 months, and at least annually thereafter. In a subject with an increased risk of PCa urologist supervision is required

*An initial increase of prostate-specific antigen (PSA) and prostate volume with TTh is frequently seen over the first 2–6 months because the prostate is an androgen-dependent organ. The increase in PSA will be greatest in men with marked TD and least (or absent) in men with milder degrees of TD. The PSA level at 6 months after initiation of TTh should be used as the new baseline

*Referral to a urologist for prostate evaluation and possible biopsy during TTh should be made with the development of a new palpable prostate abnormality on DRE or with a worrisome rise in PSA. Recommendations regarding what constitutes a concerning rise in PSA include an increase of 1.0 ng/ml over baseline PSA or a PSA velocity greater than 0.35 ng/ml per year.





EAU Guidelines on Sexual and Reproductive health 2023

3.7 Safety and follow-up in hypogonadism management


3.7.3 Lower urinary tract symptoms/benign prostatic hyperplasia

Based on the assumption that prostate growth is dependent on the presence of androgens, historically testosterone therapy has raised some concerns regarding the possibility of aggravating LUTS in patients affected by benign prostatic hyperplasia (BPH) associated with prostate enlargement [100, 144]. However, pre-clinical and clinical data have indicated that low rather than high androgen levels may decrease bladder capacity, alter tissue histology and decrease the ratio of smooth muscle to connective tissue, thus impairing urinary dynamics [100, 144].

A trial of 60 patients undergoing testosterone therapy for six months showed no significant differences in post-void residual urine and prostate volume, while storage symptoms as measured by IPSS significantly improved, despite an increase in prostate-specific antigen (PSA) level [145]. A larger pre-treatment prostate volume was a predictive factor of improvement in LUTS. Similarly, a placebo controlled RCT including 120 hypogonadal (total testosterone < 12 nmol/L) men with MetS waitlisted for BPH surgery, showed that testosterone therapy did not result in a difference in in LUTS severity compared to placebo. Conversely, an improvement in ultrasound markers of inflammation in the expression of several pro-inflammatory genes was found in the treatment active arm [146]. A long-term study of 428 men undergoing testosterone therapy for 8 years demonstrated significant improvements in IPSS, no changes max flow rate (Qmax) and residual urine volume, but also a significant increase in prostate volume [147]. Similar data from the Registry of Hypogonadism in Men (RHYME), including 999 patients with a follow-up of 3 years, did not document any significant difference in PSA levels or total IPSS in men undergoing testosterone therapy, compared to untreated patients [148]. Similar results were reported in an Italian registry (SIAMO-NOI), collecting data from 432 hypogonadal men from 15 centres [149]. Meta-analyses have not found significant changes in LUTS between patients treated with testosterone or placebo [150-156]. According to the most recent literature, there are no grounds to discourage testosterone therapy in hypogonadal patients with BPH/LUTS and there is evidence of limited benefit from androgen administration. The only concern is related to patients with severe LUTS (IPSS > 19), as they are usually excluded from RCTs, therefore limiting the long-term safety data of testosterone therapy in this specific setting [100].




3.7.4 Prostate cancer (PCa)

A considerable number of observational studies have failed to demonstrate any association between circulating higher testosterone levels and PCa [157]. In contrast, studies investigating the relationship between low levels of testosterone and risk of PCa have found that men with very low levels of fT have a reduced risk of developing low-to-intermediate-grade PCa, but have a non-significantly increased chance of developing highgrade PCa [157]. This peculiar pattern was also reported in trials such as the Health Professionals Follow-up Study, the Prostate Cancer Prevention Trial (PCPT) and the Reduction by Dutasteride of Prostate Cancer Events (REDUCE), with varying magnitudes of significance [158].

The most recent meta-analysis, including 27 placebo-controlled, RCTs, found no evidence of increased PSA levels following testosterone therapy for one year. When considering 11 studies reporting on the occurrence of PCa, the meta-analysis found no evidence of increased risk of PCa. However, a 1-year follow-up may be considered too short to draw firm conclusions on the risks of developing PCa. Furthermore, the analysis was restricted to studies with > 1-year follow-up, but no significant changes in PSA levels nor increased risk of PCa were found [151]. After 5-years’ median follow-up in three independent registry studies with > 1,000 patients undergoing testosterone therapy, PCa occurrence remained at all times below the reported incidence rate in the general population [159]. Similar results were reported by a more recent large observational study including 10,311 men treated with testosterone therapy and 28,029 controls with a median follow-up of 5.3 years [160]. The same study, also showed that the risk of PCa was decreased for men in the highest tertile of testosterone therapy cumulative dose exposure as compared with controls [160]

With regards to PCa survivors, safety in terms of the risk of recurrence and progression has not yet been established. Limited data are available in the literature, with most case series not providing sufficient data to draw definitive conclusions (e.g., insufficient follow-up, small samples, lack of control arms, heterogeneity in study population and treatment regimen, etc.) [161]. More recently, a meta-analysis derived from 13 studies including 608 patients, of whom 109 had a history of high-risk PCa, with follow-up of 1-189.3 months [162], suggested that testosterone therapy did not increase the risk of biochemical recurrence, but the available evidence is poor, limiting data interpretation [162]. Similar considerations can be derived from another, larger meta-analysis of 21 studies [163]. It is important to recognise that most of the studies analysed included lowrisk patients with Gleason score < 8 [162]. Interestingly, Valderrábano et al., recently described the design of the first RCT which assessed the safety/benefit ratio of testosterone therapy in hypogonadal men successfully treated with prostatectomy for non-aggressive prostate cancer [164]. The study is still ongoing and eligible subjects are randomized to testosterone cypionate (100 mg/week) or placebo for 12 weeks, followed by another 12 weeks.

In conclusion, recent literature does not support an increased risk of PCa in hypogonadal men undergoing testosterone therapy. Although it is mandatory to avoid testosterone administration in men with advanced PCa, insufficient long-term prospective data on the safety of androgen administration in PCa survivors [163], without recurrence should prompt caution in choosing to treat symptomatic hypogonadal men in this setting. Specifically, patients should be fully counselled that the long-term effects of testosterone therapy in this setting are still unknown and requires further investigation. If an occult PCa is not detected before initiation of testosterone therapy, treatment may unmask the cancer detected by an early rise in PSA over 6-9 months of therapy. Due to the lack of strong evidence-based data on safety, the possible use of testosterone therapy in symptomatic hypogonadal men previously treated for PCa should be fully discussed with patients and limited to low-risk individuals.

 

[Jake_from_StateFarm]

Thanks for the replies. I don't recollect any discussion regarding pulsing to the 400mg to 600mg range. I was wondering if it was more along Taeian Clark's recommendation of 10% to 20% above therapeutic TRT dosage.

 

[madman]

Thanks for the replies. I don't recollect any discussion regarding pulsing to the 400mg to 600mg range. I was wondering if it was more along Taeian Clark's recommendation of 10% to 20% above therapeutic TRT dosage.

Again having healthy FT levels is what matters.

Most men on trt are injecting 100-200 mg T/week.

Even than most would never need the higher-end dose.

The majority of men can easily achieve a healthy let alone high trough FT level injecting 100-150 mg T/week especially when split into more frequent injections.