High testosterone is like … finasteride? Say what!

[Cataceous]

It’s not quite as off-the-wall as it sounds. We know that as serum testosterone increases the 5α-reductase enzyme starts to saturate, leading to a reduced efficiency in DHT creation, illustrated thusly:

Even so, with high testosterone a lack of DHT is not going to be a problem; there’s still going to be a lot of it, likely at supraphysiological levels. A T/DHT imbalance is possible, though this would seem to be a more subtle problem.

However, what’s going on with other 5α-reductase-mediated processes? It seems possible that there are deleterious effects on these processes through competitive inhibition that increases with the level of testosterone. For example, there may be a reduction in the conversion of progesterone to dihydroprogesterone. This is cited as one of the possible reasons for finasteride-induced side effects. Clearly the overall effect is going to be less dramatic, as lack of DHT is likely a significant factor when finasteride is in play. Additionally, the effects on 5α-reductase activity from competitive inhibition are likely less drastic than those from finasteride. Nonetheless, with individual variability it seems plausible that some men will experience problems from this, which serves as a further reminder that high levels of testosterone are not necessarily benign.

Some comments by ChatGPT:

In summary, it is entirely plausible that high levels of serum testosterone can competitively inhibit the conversion of other steroid substrates by 5α-reductase, including the conversion of progesterone to dihydroprogesterone. The structural similarities and abundance of testosterone in such scenarios create a scenario ripe for competitive inhibition. This is a fascinating area of research with potential implications for understanding various physiological and pathological conditions. …​

To be fair, it does mention some caveats:

• Complexity: Hormonal regulation is highly complex, and many factors can influence the activity of 5α-reductase. This isn’t a simple “one substrate wins” scenario.​

​

• Feedback Mechanisms: The body has negative feedback loops to regulate hormone production, so simply increasing testosterone wouldn’t necessarily cause a sustained reduction in other 5α-reductase products.​

​

• Tissue Specificity: The effects could be tissue-specific since the levels and forms of 5α-reductase vary throughout the body.​

 

[Nelson Vergel]

We have had data about how exogenous testosterone can decrease upstream neurosteroids. I am sure that decrease is worse at higher T doses.

Anabolic steroids and TRT decrease SHBG, DHEA, pregnenolone and progesterone in men.

Effects of Anabolic Steroids and Testosterone on Hormonal Function in Power Athletes A study published in The Journal of Steroid Biochemistry (1985) investigated the effects of self-administered high doses of testosterone and anabolic steroids on testicular endocrine function and circulating...

www.excelmale.com

Allopregnanolone is one of the most important neurosteroids involved in mood. It is dependent on 5 alpha reductase.

Allopregnanolone in mood disorders

ABSTRACT The neuroactive steroid allopregnanolone (ALLO) is an endogenous positive allosteric modulator of GABA type A receptor (GABAAR), and the down-regulation of its biosynthesis has been attributed to the development of mood disorders, such as depression, anxiety, and post-traumatic stress...

www.excelmale.com

I searched on perplexity:

The effect of supraphysiologic testosterone on allopregnanolone levels in men is complex and involves several interrelated mechanisms:

## Neurosteroid Biosynthesis

Supraphysiologic testosterone administration can lead to changes in neurosteroid biosynthesis, particularly affecting allopregnanolone levels:

1. **Decreased Allopregnanolone**: Long-term administration of high doses of testosterone has been associated with a decrease in brain allopregnanolone content[1][4]. This reduction is likely due to the down-regulation of neurosteroid biosynthesis pathways.

2. **5α-reductase Expression**: Testosterone administration can cause a decrease in the expression of 5α-reductase type I mRNA, which is a key enzyme in the biosynthesis of allopregnanolone[1][4]. This decrease in enzyme expression contributes to the reduced allopregnanolone levels.

## Behavioral Effects

The changes in allopregnanolone levels due to supraphysiologic testosterone can have significant behavioral implications:

1. **Aggression**: The decrease in brain allopregnanolone content has been associated with increased aggressive behavior[1][4]. This may partly explain the phenomenon of "steroid rage" observed in some individuals using anabolic-androgenic steroids.

2. **Mood Alterations**: Allopregnanolone is a potent modulator of GABA_A receptors, and its reduction can lead to changes in mood, potentially contributing to irritability and anxiety[3].

## Compensatory Mechanisms

The body may attempt to compensate for the effects of supraphysiologic testosterone:

1. **Androgen Backdoor Pathway**: Allopregnanolone is an intermediate in an androgen backdoor pathway from progesterone to dihydrotestosterone[3]. This pathway may be affected by supraphysiologic testosterone levels, potentially altering allopregnanolone production.

2. **Intratumoral Testosterone**: In the context of prostate cancer, long-term androgen deprivation therapy can lead to similar or even higher intratumoral testosterone levels compared to pre-castrate levels[2]. This suggests complex regulatory mechanisms that may also influence allopregnanolone synthesis.

## Clinical Implications

Understanding the relationship between supraphysiologic testosterone and allopregnanolone has important clinical implications:

1. **Cognitive Function**: Both testosterone and allopregnanolone play roles in cognitive function. Alterations in their levels may impact cognitive performance in older men[6].

2. **Sexual Function**: Changes in neurosteroid levels, including allopregnanolone, can affect sexual function. The neurosteroid androsterone, which is related to allopregnanolone in the steroid biosynthesis pathway, has been correlated with sexual interest in men[7].

3. **Prostate Cancer Treatment**: Supraphysiological testosterone therapy has shown potential in treating certain cases of enzalutamide-resistant prostate cancer[8]. The effects on allopregnanolone in this context warrant further investigation.

In conclusion, supraphysiologic testosterone administration in men can lead to a decrease in allopregnanolone levels through down-regulation of neurosteroid biosynthesis pathways. This change can have significant effects on behavior, mood, and potentially cognitive function. However, the body's compensatory mechanisms and the complex interplay between different steroid hormones make this relationship nuanced and context-dependent.

Citations:
[1] Changes in brain testosterone and allopregnanolone biosynthesis elicit aggressive behavior - PubMed
[2] https://erc.bioscientifica.com/view/journals/erc/24/11/ERC-17-0155.xml
[3] Allopregnanolone - Wikipedia
[4] Changes in brain testosterone and allopregnanolone biosynthesis elicit aggressive behavior - PMC
[5] Effects of Progesterone and Testosterone on Cocaine Self-Administration and Cocaine Discrimination by Female Rhesus Monkeys - Neuropsychopharmacology
[6] Frontiers | An Updated Review: Androgens and Cognitive Impairment in Older Men
[7] https://jamanetwork.com/journals/jamapsychiatry/fullarticle/209516
[8] https://www.europeanurology.com/article/S0302-2838(19)30449-X/fulltext

 

[Seagal]

It’s not quite as off-the-wall as it sounds. We know that as serum testosterone increases the 5α-reductase enzyme starts to saturate, leading to a reduced efficiency in DHT creation, illustrated thusly:

View attachment 49552
Even so, with high testosterone a lack of DHT is not going to be a problem; there’s still going to be a lot of it, likely at supraphysiological levels. A T/DHT imbalance is possible, though this would seem to be a more subtle problem.

However, what’s going on with other 5α-reductase-mediated processes? It seems possible that there are deleterious effects on these processes through competitive inhibition that increases with the level of testosterone. For example, there may be a reduction in the conversion of progesterone to dihydroprogesterone. This is cited as one of the possible reasons for finasteride-induced side effects. Clearly the overall effect is going to be less dramatic, as lack of DHT is likely a significant factor when finasteride is in play. Additionally, the effects on 5α-reductase activity from competitive inhibition are likely less drastic than those from finasteride. Nonetheless, with individual variability it seems plausible that some men will experience problems from this, which serves as a further reminder that high levels of testosterone are not necessarily benign.

Some comments by ChatGPT:

In summary, it is entirely plausible that high levels of serum testosterone can competitively inhibit the conversion of other steroid substrates by 5α-reductase, including the conversion of progesterone to dihydroprogesterone. The structural similarities and abundance of testosterone in such scenarios create a scenario ripe for competitive inhibition. This is a fascinating area of research with potential implications for understanding various physiological and pathological conditions. …​

To be fair, it does mention some caveats:

• Complexity: Hormonal regulation is highly complex, and many factors can influence the activity of 5α-reductase. This isn’t a simple “one substrate wins” scenario.​

​

• Feedback Mechanisms: The body has negative feedback loops to regulate hormone production, so simply increasing testosterone wouldn’t necessarily cause a sustained reduction in other 5α-reductase products.​

​

• Tissue Specificity: The effects could be tissue-specific since the levels and forms of 5α-reductase vary throughout the body.​

Tissue specificity.
I don't believe that the observed saturation is due to enzyme exhaustion. There must be more feedback loops.

However, I support the slow and low approach to TRT.
Again, we need more basic research...

 

[Cataceous]

Tissue specificity.
I don't believe that the observed saturation is due to enzyme exhaustion. There must be more feedback loops.
...

If you're interested in the details, here's the study containing the graph. They say:

Modeling the free E2 vs. free testosterone and free DHT vs. free testosterone relationships showed that our data are consistent with Michaelis-Menten enzyme kinetics in both cases.​

Michaelis–Menten kinetics - Wikipedia

en.wikipedia.org

Further addition of substrate would not increase the rate, and the enzyme is said to be saturated.​

 

[Seagal]

If you're interested in the details, here's the study containing the graph. They say:

Modeling the free E2 vs. free testosterone and free DHT vs. free testosterone relationships showed that our data are consistent with Michaelis-Menten enzyme kinetics in both cases.​

Michaelis–Menten kinetics - Wikipedia

en.wikipedia.org

Further addition of substrate would not increase the rate, and the enzyme is said to be saturated.​

Thank you Cataceous. I was positively surprised about the statistics. The biostatistics department was on board.
I will read in more detail... Figure 1 free DHT seems to double when going from 300 to 600mg T.
What I assumed with my previous post is that over time enzymatic conversion* would slowly adjust (similar to the honeymoon period).
* "Vmax represents the limiting rate approached by the system at saturating substrate concentration for a given enzyme concentration".
The authors measured T and metabolites every month for 5 months. I suppose they would have mentioned if there was a time-dependent change in metabolites and ratios, or not, since they aimed to compare young vs old men.

Wikipedia
"Only a small proportion of enzyme-catalysed reactions have just one substrate, but the equation still often applies if only one substrate concentration is varied."

 

[Vince]

If you're interested in the details, here's the study containing the graph. They say:

Modeling the free E2 vs. free testosterone and free DHT vs. free testosterone relationships showed that our data are consistent with Michaelis-Menten enzyme kinetics in both cases.​

Michaelis–Menten kinetics - Wikipedia

en.wikipedia.org

Further addition of substrate would not increase the rate, and the enzyme is said to be saturated.​

Here's a copy of 2010 control trial.
Background: During testosterone (T) therapy, T is partly converted to 17beta-estradiol (E2) and 5alpha-dihydrotestosterone (DHT). Effects of age, testosterone dose, and body composition on total and free E2 and DHT levels are unknown.
Objective: We evaluated age and dose-related differences in E2 and DHT levels in response to graded doses of testosterone enanthate in young and older men.
Methods: Fifty-one young (aged 19-35 yr) and 52 older (aged 59-75 yr) men completed treatment with monthly injections of a GnRH agonist plus randomly assigned weekly doses of testosterone enanthate (25, 50, 125, 300, or 600 mg) for 5 months.
Results: During testosterone administration, total and free E2 levels increased dose-dependently (dose effect, P<0.001) in both young and older men. Total and free E2 levels and E2:T ratios during T administration were higher in older than young men, but age-related differences in free E2 and free E2:T ratios were not significant after adjusting for testosterone levels, percentage fat mass, and SHBG. DHT levels and DHT:T ratios were dose-related but did not differ between young and older men. Mechanistic modeling of free hormone data revealed that the conversions of T to E2 and DHT were both consistent with saturable Michaelis-Menten kinetics. The in vivo Km values were estimated to be 1.83 nm for aromatase and 3.35 nm for 5alpha-reductase, independent of age. The Vmax parameter for E2 was 40% higher in older men than younger men, but Vmax for DHT was not significantly different between age groups.
Conclusions: During im testosterone administration, E2 and DHT levels exhibit saturable increases with dose. The rate of whole body aromatization is higher in older men, partly related to their higher percentage fat mass, SHBG, and testosterone levels.

 

[Vince]

If you're interested in the details, here's the study containing the graph. They say:

Modeling the free E2 vs. free testosterone and free DHT vs. free testosterone relationships showed that our data are consistent with Michaelis-Menten enzyme kinetics in both cases.​

Michaelis–Menten kinetics - Wikipedia

en.wikipedia.org

Further addition of substrate would not increase the rate, and the enzyme is said to be saturated.​

Here's the full text link to 2010 trial.

The Effects of Injected Testosterone Dose and Age on the Conversion of Testosterone to Estradiol and Dihydrotestosterone in Young and Older Men - PMC

Background: During testosterone (T) therapy, T is partly converted to 17β-estradiol (E2) and 5α-dihydrotestosterone (DHT). Effects of age, testosterone dose, and body composition on total and free E2 and DHT levels are unknown. Objective: We ...

pmc.ncbi.nlm.nih.gov

 

[Gianluca]

It’s not quite as off-the-wall as it sounds. We know that as serum testosterone increases the 5α-reductase enzyme starts to saturate, leading to a reduced efficiency in DHT creation, illustrated thusly:

View attachment 49552
Even so, with high testosterone a lack of DHT is not going to be a problem; there’s still going to be a lot of it, likely at supraphysiological levels. A T/DHT imbalance is possible, though this would seem to be a more subtle problem.

However, what’s going on with other 5α-reductase-mediated processes? It seems possible that there are deleterious effects on these processes through competitive inhibition that increases with the level of testosterone. For example, there may be a reduction in the conversion of progesterone to dihydroprogesterone. This is cited as one of the possible reasons for finasteride-induced side effects. Clearly the overall effect is going to be less dramatic, as lack of DHT is likely a significant factor when finasteride is in play. Additionally, the effects on 5α-reductase activity from competitive inhibition are likely less drastic than those from finasteride. Nonetheless, with individual variability it seems plausible that some men will experience problems from this, which serves as a further reminder that high levels of testosterone are not necessarily benign.

Some comments by ChatGPT:

In summary, it is entirely plausible that high levels of serum testosterone can competitively inhibit the conversion of other steroid substrates by 5α-reductase, including the conversion of progesterone to dihydroprogesterone. The structural similarities and abundance of testosterone in such scenarios create a scenario ripe for competitive inhibition. This is a fascinating area of research with potential implications for understanding various physiological and pathological conditions. …​

To be fair, it does mention some caveats:

• Complexity: Hormonal regulation is highly complex, and many factors can influence the activity of 5α-reductase. This isn’t a simple “one substrate wins” scenario.​

​

• Feedback Mechanisms: The body has negative feedback loops to regulate hormone production, so simply increasing testosterone wouldn’t necessarily cause a sustained reduction in other 5α-reductase products.​

​

• Tissue Specificity: The effects could be tissue-specific since the levels and forms of 5α-reductase vary throughout the body.​

I remember commenting on this particular study here in the forum, this to be a concern for Progesterone not converting as much into allopregnenolone. Also, this study shows where the max physiological level of T are at about.

 

[Vince]

I remember commenting on this particular study here in the forum, this to be a concern for Progesterone not converting as much into allopregnenolone. Also, this study shows where the max physiological level of T are at about.

Yes, I have researched it and Allopregnanolone plays a crucial role in regulating mood, anxiety, and sleep, so a decrease in its production due to TRT could potentially contribute to mood swings or other neurological symptoms in some men.

 

[DixieWrecked]

This all makes sense to me. What is the work around if steady state of injections don't work? Scrotal cream?

 

[Gianluca]

This all makes sense to me. What is the work around if steady state of injections don't work? Scrotal cream?

This is what has been in my mind for the past few months.

I think the issue with the scrotal cream is the unphysiologic conversion of T into DHT, I’m not sure what the general thought is now about the DHT.

I would think an oral like Jatenzo would be the most physiological way to get Test into circulation.

 

[Vince]

This is what has been in my mind for the past few months.

I think the issue with the scrotal cream is the unphysiologic conversion of T into DHT, I’m not sure what the general thought is now about the DHT.

I would think an oral like Jatenzo would be the most physiological way to get Test into circulation.

I would think some men who inject 300 mg - 600 mg of T weekly will have some type of issue.

I would be scared to inject that high of dose.

 

[Cataceous]

...
I think the issue with the scrotal cream is the unphysiologic conversion of T into DHT, I’m not sure what the general thought is now about the DHT.

I would think an oral like Jatenzo would be the most physiological way to get Test into circulation.

Natesto has the evidence behind it. It's the only form of TRT proven to allow continued HPTA function, which in my mind makes it more physiological. Oral forms cause more complete suppression unless accompanied by a SERM. It's likely that appropriately dosed buccal troches would be similar in effect to the testosterone nasal gels. It's also possible that injections of a micronized testosterone suspension fit in here too, but that's a work in progress.

 

[madman]

Natesto has the evidence behind it. It's the only form of TRT proven to allow continued HPTA function, which in my mind makes it more physiological. Oral forms cause more complete suppression unless accompanied by a SERM. It's likely that appropriately dosed buccal troches would be similar in effect to the testosterone nasal gels. It's also possible that injections of a micronized testosterone suspension fit in here too, but that's a work in progress.

Doubting TS would be in the same league as Natesto when it comes to the PKs.

The daily dose used is also going to play a big role here too!


* Aqueous suspensions of sex steroids consist of tiny crystal particles of pure sex steroids that are suspended in water. These sex steroid particles are highly lipophilic and hydrophobic. When injected, the hydrophilic water vehicle is rapidly mixed into the fluid of the tissue compartment and absorbed by the body.

* But the hydrophobic sex steroid crystals are not, and instead float about in the fluid of the tissue compartment. As with oil solutions, the sex steroids at the edges of the crystals very slowly dissolve off the surface of the crystals into the surrounding water and are then distributed into the circulation and tissues. Eventually, the crystal will be fully absorbed into the body, but only after a long period of time.

* In the case of aqueous suspensions, the duration of the sex steroid is additionally highly dependent on particle size.

Post in thread 'Advice on low dose daily testosterone'

Jun 12, 2021

Although TS is unesterified the crystals of T may very well behave like small implants being more slowly absorbed from the tissues which would have an impact on the half-life.

Depending on the source the half-life given was 2 – 4 hours and some studies (animal) stating 24-39 hours.

Daily injections let alone multiple would most likely result in the shutdown HPG axis.


Andronaq (testosterone suspension)

Description:

Testosterone suspension is an injectable preparation containing testosterone (no ester), usually in a water base.


History:

Testosterone...

• madman

• 

Injectable Aqueous Suspensions

Aqueous suspensions of sex steroids also form an injection-site depot and achieve a long-lasting depot effect when administered by subcutaneous or intramuscular injection. However, they work in a completely different way than oil solutions. Aqueous suspensions of sex steroids consist of tiny crystal particles of pure sex steroids that are suspended in water. These sex steroid particles are highly lipophilic and hydrophobic. When injected, the hydrophilic water vehicle is rapidly mixed into the fluid of the tissue compartment and absorbed by the body. But the hydrophobic sex steroid crystals are not, and instead float about in the fluid of the tissue compartment. As with oil solutions, the sex steroids at the edges of the crystals very slowly dissolve off the surface of the crystals into the surrounding water and are then distributed into the circulation and tissues. Eventually, the crystal will be fully absorbed into the body, but only after a long period of time. Since the rate of absorption is dependent on lipophilicity and hydrophobicity, lipophilic esters lengthen the durations of aqueous suspensions of sex steroids by intramuscular or subcutaneous injection similarly to the case of oil solutions of sex steroids.

In the case of aqueous suspensions, the duration of the sex steroid is additionally highly dependent on particle size. These particle sizes have ranged from nanocrystalline to microcrystalline to macrocrystalline in their range. Almost always however it is microcrystalline particle sizes that have been used in injectable aqueous suspensions of sex steroids. (The present author has seen macrocrystalline preparations described a few times, specifically in research on combined injectable contraceptives (Garza-Flores, Del, & Perez-Palacios, 1992; Newton, d’Arcangues, & Hall, 1994; Sang, 1994), and is fairly sure that no such preparations have ever been marketed. On the other hand, nanocrystalline aqueous suspensions have been used with depot antipsychotics (Spanarello & Ferla, 2014; Correll et al., 2021).) Typically, there is a given particle size range for the formulation, such as 0.01 to 0.1 mm in diameter. The larger the particle sizes, the slower the absorption into the body, and the longer the duration of the preparation; the smaller the particle sizes, the faster the absorption, and the shorter the duration. When microcrystalline aqueous suspensions of sex steroids are manufactured nowadays, the particle sizes are defined and carefully controlled. Particle sizes influence the duration of injectable aqueous suspensions because they result in different surface areas from which sex steroid ester can escape particles. A single large particle has a smaller total surface area and hence dissolution rate than the same particle divided up into many smaller particles.

Particle sizes are manipulated during manufacturing via micronization—the process of decreasing the diameter of larger particles, such as via milling or grinding. Whereas more micronization improves the absorption and bioavailability of estradiol and progesterone with oral administration by increasing the surface area available for absorption into the body (Wiki; Wiki), less micronization decreases the rate of absorption of crystalline aqueous suspensions via depot injection and thereby extends the durations of these preparations by decreasing the total surface area for absorption.

There is a notable similarity of injectable aqueous suspensions of sex steroids to implantable sex steroid pellets, for instance of estradiol, testosterone, and progesterone (Wiki; Wiki; Wiki). Pellet implants are basically just pure crystalline sex steroids compressed into the shape of a small cylinder (Photo; Photo). They are inserted into subcutaneous fat in the body through a small incision using a large needle-like instrument called a trocar (Diagram). Once implanted, pellets slowly dissolve and absorb into the body over time, eventually disappearing completely. As they are nothing but pure crystalline hormones, there is no need for them to be removed or retrieved later on. In other words, implantation of a pellet is in a way the same thing as a subcutaneous injection of an aqueous suspension of sex steroid crystals—a single pellet is just one massive crystal instead of many tiny crystals suspended in water. And with very large crystals comes a very long duration—typically 6 months or more for each subcutaneous pellet of estradiol or testosterone (Kuhl, 2005; Wiki; Wiki). However, though injectable aqueous suspensions are typically much less prolonged than pellet implants, they have the advantages over pellets of being less expensive and not requiring a surgical incision. Due to the similarity between aqueous suspensions and pellet implants, aqueous suspensions have been described and marketed as “micropellets” in the past.

Thread 'Suppression of Serum LH and FSH in Adult Males following Exogenous Testosterone Suspension Administration (1972)'

Mar 1, 2025

* Samples of venous blood were obtained from 22 healthy adult males age 19-26 before and after the im injection of testosterone in aqueous suspension (Oreton©).


* The administration of the 12.5 and 25.0 mg of testosterone daily was reflected by markedly higher levels of serum testosterone. After the third dose of 25.0 mg, this level reached a peak within 16 hr after im administration and remained above control levels for at least 24 hr after the higher doses were administered. The rate of decline and the magnitude and duration of depression below...

• madman
• testosterone; gonadotropins; lh/fsh; hpta
• Replies: 2
• Forum: Testosterone and Men's Health Articles

• 

 

[Gianluca]

I would think some men who inject 300 mg - 600 mg of T weekly will have some type of issue.

I would be scared to inject that high of dose.

For sure

 

[Gianluca]

as far as pharmacokinetics, if I remember correctly, scrotal cream applied once per day only is the closet to mimic endogenous T production. Too bad the DHT issue classify it far away from physiologic to me.

 

[Vince]

as far as pharmacokinetics, if I remember correctly, scrotal cream applied once per day only is the closet to mimic endogenous T production. Too bad the DHT issue classify it far away from physiologic to me.

Plus my issue with cream is contaminating my wife or grandkids.

 

[Gianluca]

Plus my issue with cream is contaminating my wife or grandkids.

@Vince Are you still injecting everyday IM?

 

[madman]

as far as pharmacokinetics, if I remember correctly, scrotal cream applied once per day only is the closet to mimic endogenous T production. Too bad the DHT issue classify it far away from physiologic to me.

No that title would go to the T-patch (Androderm) applied before bed!

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.

Thread 'ANDRODERM® (TDS)'

Aug 7, 2021

About Androderm® (testosterone transdermal system) | Learn About the Androderm Patch®

Learn more about the Androderm® patch, including usage and spreading testosterone. View Important Risk Information and full Prescribing Information on the website.

www.androderm.com

ANDRODERM® (testosterone transdermal system) is designed to deliver testosterone continuously for 24 hours following application to intact, non-scrotal skin (e.g., back, abdomen, thighs, upper arms).

Four strengths of ANDRODERM® are available that deliver approximately 2 mg, 2.5 mg, 4 mg, or 5 mg of testosterone per day. ANDRODERM® has a central drug delivery reservoir surrounded by a peripheral adhesive area.

The ANDRODERM® 2 mg/day system has a total contact surface area of 32 cm 2 with a 6.0 cm 2 central...

• madman
• t-patch/androderm
• Replies: 6
• Forum: Testosterone and Men's Health Articles

• 

Post in thread 'Labcorp VS Quest'

May 10, 2024

Your question is on a pretty unrelated topic thread. Might start a new thread with this question.

I know members here have done both morning/evening, and injection/cream combos. I have done both and cream does not work well for me period. I was never fully satisfied with straight T cyp, and was glad to find @Cataceous ratio of 4 parts cypionateor enanthate to 3 parts proprionate by weight. I mix the esters in a sterile vial and inject a small dose daily. The prop gives a bit of peak/trough each day, but the enanthate keeps the base/trough level high enough. Mimics a daily...

• madman

Post in thread 'T.Cyp 100 mg/week - Night sweats, anxiety'

Oct 8, 2023

This is good advice. More frequent injections never worked for me either. Always made me feel like complete crap. High resting heart rate, insomnia, moody, sexual side effects. And many more. With esters like cypionate , and enanthate you don’t need to inject more often. The problem with more often injections is that your levels are always peaked. That’s not healthy at all. The body needs fluctuations. Injecting every day or every other day does not mimic natural production at all. All that advice is just based on bro science B.S.

With esters...

• madman

• 

Post in thread 'So who is happy with TRT? Who wish they never started?'

Sep 19, 2023

I've been following your journey for a few years and it's great that oral T is working! I was reading an abstract on steroidogenesis and the authors stated that oral forms of testosterone closely mimic the daily peaks and troughs of endogenous testosterone.

I looked up the inactive ingredients in Jatenzo and not sure it or any other oral form is for me because of my many chemical sensitivities. I'm a walking disaster in that regard, LOL.

If anything you are getting 2 daily peak/troughs 24/7.

T levels will be much lower before it is time for your second dose (12 hrs...

• madman

• 

 

[Vince]

@Vince Are you still injecting everyday IM?

Yes, I'm still doing daily injections. Shallow IM and SubQ.