Nandrolone added to TRT to reduce DHT?

[bp]

I would appreciate any professional opinion on adding nandrolone to TRT to help attenuate high DHT symptoms, specifically acne.

For example;

If the current protocol was 100mg of a testosterone ester per week.

With the protocol being ideal, but for the acne due to DHT conversion.
Would 'exchanging' 30mg of the testosterone ester for 30mg of a nandrolone ester (of similar weight, so that the resulting nandrolone at the depot site is basically equal in dosage to the 'swapped testosterone' after being dehydrolysed) lessen the acne issue due to Nandrone being a non DHT derivative 19nor test ?
So in essence, the total dosage would be the same (100mg per week). However only 70mg being able to convert to DHT
Any feedback from you gentlemen would be greatly received.

 

[Vince]

I would appreciate any professional opinion on adding nandrolone to TRT to help attenuate high DHT symptoms, specifically acne.

For example;

If the current protocol was 100mg of a testosterone ester per week.

With the protocol being ideal, but for the acne due to DHT conversion.
Would 'exchanging' 30mg of the testosterone ester for 30mg of a nandrolone ester (of similar weight, so that the resulting nandrolone at the depot site is basically equal in dosage to the 'swapped testosterone' after being dehydrolysed) lessen the acne issue due to Nandrone being a non DHT derivative 19nor test ?
So in essence, the total dosage would be the same (100mg per week). However only 70mg being able to convert to DHT
Any feedback from you gentlemen would be greatly received.

Can you post your DHT levels along with the ranges?

 

[Gman86]

Theoretically, this should work. Nandrolone produces DHN, which is like a weaker form of DHT. I’ve been talking to a lot of guys using nandrolone as their base, with small doses of test to boost E2 up a bit. I’m pretty sure all of them report less acne and bloating. A few of them have actually reported that the hair on their head got thicker. So if you’re having any issues due to high DHT or high E2, what you plan on doing should work quite well. You’re going to be lowering DHT and E2, while actually having slightly more androgen receptor activation than on 100mg of test. Nandrolone is 25% more anabolic than testosterone. So by using 70mg of test, and 30mg of nandrolone, you’ll have a slightly higher anabolic response, while slightly decreasing E2 and DHT. Theoretically I’d say this experiment should result in a win win.

 

[Gman86]

@bp Man, just saw your post on the fb group. You got eaten alive over there lol. I would personally just give your idea a shot, and see if it helps. At the end of the day, nobody knows exactly what’s going to happen, and how your body is going to react. Everyone’s just speculating, including me. If I were you, I would personally try it. Theoretically, your plan makes sense, imo.

 

[madman]

I would appreciate any professional opinion on adding nandrolone to TRT to help attenuate high DHT symptoms, specifically acne.

For example;

If the current protocol was 100mg of a testosterone ester per week.

With the protocol being ideal, but for the acne due to DHT conversion.
Would 'exchanging' 30mg of the testosterone ester for 30mg of a nandrolone ester (of similar weight, so that the resulting nandrolone at the depot site is basically equal in dosage to the 'swapped testosterone' after being dehydrolysed) lessen the acne issue due to Nandrone being a non DHT derivative 19nor test ?
So in essence, the total dosage would be the same (100mg per week). However only 70mg being able to convert to DHT
Any feedback from you gentlemen would be greatly received.

Acne is much more complex than simply DHT levels.

DHT is not the sole contributor to whether one will experience such.

Genetics /sensitivity of the AR to androgens/DHT play a big role.

Genetically prone individuals can still experience acne even when using lower doses of testosterone.




What is new in the pathophysiology of acne, an overview

Error - Cookies Turned Off


Introduction
Acne is a chronic inflammatory disease of the pilosebaceous unit.1 It commonly occurs at puberty but is also observed in adults.2 Its pathophysiology involves three actors, hyper-seborrhoea, abnormal follicular keratinization and Propionibacterium acnes proliferation in the pilosebaceous unit. As a result of their interaction, the cutaneous microenvironment changes and leads to inflammatory reactions of the host that foster acne lesion progression.2, 3 Recent research has put some new light on the involvement of the sebaceous gland, as well as on the pro‐inflammatory activity of the cutaneous microbiome in the pathophysiology of acne.

The objective of this article was to provide an update regarding the involvement of the sebaceous gland, the innate immunity and the cutaneous microbiome in acne. The second objective was to open a new perspective of treatment options.



The sebaceous gland
Sebum production is induced by different receptors expressed by the sebaceous gland. In addition to the well‐described histamine receptor activated by histamines, the hormonal DHT receptor, activated by androgens, and the neuromodulator receptor, mainly substance P and corticotrophin‐releasing hormone (CRH) receptor which are mainly activated by stress, recent molecular research has identified three other receptors that are expressed by the sebocyte and that control sebum production (Fig. 1).4-6

FIGURE 1

Receptors controlling sebum production (adapted from Zhang et al.7).


Each of these newly identified receptors is activated by a dietary substance. The peroxisome proliferator‐activated receptors (PPARα, β and γ) are stimulated by free fatty acids and cholesterol, the insulin‐like growth factor (IGF)‐1 receptor by sugar and leptin receptor by fat.7-9 Leptin is a hormone secreted by adipocytes that regulates bodyweight and is also known to link lipid metabolism with inflammation in various cell types. In the sebocyte, it is responsible for creating lipid droplets within the cell and has recently been shown to induce pro‐inflammatory enzyme and cytokine (interleukin (IL)‐6 and IL‐8) secretion as well.9 This result suggests that leptin is a novel player in inducing inflammation and altering lipid profile in sebocytes and could be a link between diet and development of inflammatory acne.

The link between acne and diet is further supported by a recent case–control study of predictive factors for acne.10 Apart from the well‐known relationship between family history and acne, the investigators found that a high body mass index (BMI) was also a predictive factor for an increased risk of developing moderate to severe acne in adolescents and young adults. Furthermore, a population‐based study of acne and BMI in adolescents reported that overweight as well as obesity may be potentially associated with acne in girls aged 18 and 19 years,11 even though proofs are still lacking.






Dihydrotestosterone: Biochemistry, Physiology, and Clinical Implications of Elevated Blood Levels

Dihydrotestosterone: Biochemistry, Physiology, and Clinical Implications of Elevated Blood Levels


Skin
Skin possesses all of the requisite steroidogenic capabilities to ensure local homeostatic control of steroid hormones, suggesting an important paracrine role for T, DHT, and estradiol within the skin, the function of which is poorly understood (143). Likewise, skin contains metabolizing pathways (e.g., glucuronidation; sulphation) that inactivate DHT (144). Consequently, localized mechanisms in skin maintain concentrations of DHT that are not meaningfully influenced by circulating DHT levels, probably due to the fact that the DHT concentration gradient favors secretion into blood (143, 145). In men, androgen levels are highest in the scrotal skin followed by pubic skin and then thigh skin, a pattern paralleled by 5α-reductase and low 3α-reductase activity (and thus tissue DHT) (146). In women, skin DHT concentrations are highest in the labia majora and clitoris followed by pubic skin and then thigh skin (147).

Absorption of DHT (as is also true for T) across the skin is a passive process that follows Fick’s law (148, 149). Accordingly, concentrations of DHT in skin to which DHT has been applied are extremely high during the period when DHT is absorbed into the bloodstream. A single transdermal DHT product is available in a handful of countries, and it is this formulation that has been used in clinical trials. Studies of topical DHT in hypogonadal or eugonadal men have not reported adverse effects on skin aside from mild irritation due to the high alcohol content, despite its direct application and sustained supraphysiological levels of DHT for up to 24 months (51, 52, 54). These results are consistent with those from shorter-term transdermal DHT studies (60, 103).

Male human skin and hair express an abundance of SRD5A type I in sebaceous glands, hair follicles, sweat glands, and the epidermis, whereas SRD5A type II is expressed in genital keratinocytes and hair follicles (150). The physiologic role of DHT in the skin is unclear, but it is hypothesized that sex steroids may influence the immune function of skin and locally influence inflammatory processes (143). Androgens clearly play a role in the pathogenesis of acne vulgaris, likely through increased sebum production, and may impact cutaneous wound healing (151); however, a specific role for DHT in many of these processes has not been demonstrated. An exception to this may be DHT-induced upregulation of inflammatory cytokines (e.g., IL-1, IL-6, and tumor necrosis factor-α) in acne (152). Studies of agents that reduce levels of DHT in skin clearly support a role for DHT in the development of male androgenic alopecia (MAA) (male pattern baldness). This is inferred, in part, by the effectiveness of 5AR-Is in suppressing the progression of MAA and the observations that castrated men and men with SRD5A deficiency do not develop baldness (153). However, the effectiveness of SRD5A therapy likely resides at the level of the hair follicle (i.e., lowered follicular concentrations of DHT) and not a reduction of circulating DHT because this has not been shown to correlate with MAA. Support for this conclusion is also found in a study of men exposed to exceptionally high levels of DHT in response to daily application of a DHT gel preparation for 24 months. DHT was not associated with acne, MAA, or other androgen-associated skin pathology (54). Instead, the most important factor in the pathogenesis of MAA is a genetic predisposition for AR polymorphisms [e.g., synonymous nucleotide polymorphism in exon 1 (rs6152) of the AR] (154, 155). In addition, differences in AR concentrations and steroid-converting enzymes in the hair follicle also appear to be play a significant role in MAA (156).

 

[madman]

@bp Man, just saw your post on the fb group. You got eaten alive over there lol. I would personally just give your idea a shot, and see if it helps. At the end of the day, nobody knows exactly what’s going to happen, and how your body is going to react. Everyone’s just speculating, including me. If I were you, I would personally try it. Theoretically, your plan makes sense, imo.

Is this really anyone's business to know on this forum!

 

[madman]

Can you post your DHT levels along with the ranges?

Great point as we have no idea where his DHT levels sit on such protocol.

Mind you I would me more interested in testing free DHT levels but even than what truly matters is (statements below).


"Circulating levels of DHT in response to testosterone replacement therapy (TRT) do not correlate with those found in androgen sensitive tissue (e.g., prostate, adipose, muscle) due to local regulatory mechanisms that tightly control intracellular androgen homeostasis"

"We are reminded of Horton’s admonition some 25 years ago when he concluded
that blood levels of DHT provide only a hint of tissue levels and that DHT should be regarded as a paracrine hormone formed and acting primarily within target tissues (39)."

 

[madman]

I would appreciate any professional opinion on adding nandrolone to TRT to help attenuate high DHT symptoms, specifically acne.

For example;

If the current protocol was 100mg of a testosterone ester per week.

With the protocol being ideal, but for the acne due to DHT conversion.
Would 'exchanging' 30mg of the testosterone ester for 30mg of a nandrolone ester (of similar weight, so that the resulting nandrolone at the depot site is basically equal in dosage to the 'swapped testosterone' after being dehydrolysed) lessen the acne issue due to Nandrone being a non DHT derivative 19nor test ?
So in essence, the total dosage would be the same (100mg per week). However only 70mg being able to convert to DHT
Any feedback from you gentlemen would be greatly received.

You could try lowering the test dose slightly but again depends on where your TT/FT and e2 levels sit on current dose 100 mg/week.

Doubtful replacing the dose reduction of T with 30 mg/week of nandrolone is going to have a drastic impact.....but no harm in giving it a go.

If your TT/FT and e2 levels are high enough on current protocol and you truly have room to bring them down some than I would at least try dropping your weekly test dose from 100--->70 mg/week first before adding in the nandrolone.

 

[bp]

Acne is much more complex than simply DHT levels.

DHT is not the sole contributor to whether one will experience such.

Genetics /sensitivity of the AR to androgens/DHT play a big role.

Genetically prone individuals can still experience acne even when using lower doses of testosterone.




What is new in the pathophysiology of acne, an overview

Error - Cookies Turned Off


Introduction
Acne is a chronic inflammatory disease of the pilosebaceous unit.1 It commonly occurs at puberty but is also observed in adults.2 Its pathophysiology involves three actors, hyper-seborrhoea, abnormal follicular keratinization and Propionibacterium acnes proliferation in the pilosebaceous unit. As a result of their interaction, the cutaneous microenvironment changes and leads to inflammatory reactions of the host that foster acne lesion progression.2, 3 Recent research has put some new light on the involvement of the sebaceous gland, as well as on the pro‐inflammatory activity of the cutaneous microbiome in the pathophysiology of acne.

The objective of this article was to provide an update regarding the involvement of the sebaceous gland, the innate immunity and the cutaneous microbiome in acne. The second objective was to open a new perspective of treatment options.



The sebaceous gland
Sebum production is induced by different receptors expressed by the sebaceous gland. In addition to the well‐described histamine receptor activated by histamines, the hormonal DHT receptor, activated by androgens, and the neuromodulator receptor, mainly substance P and corticotrophin‐releasing hormone (CRH) receptor which are mainly activated by stress, recent molecular research has identified three other receptors that are expressed by the sebocyte and that control sebum production (Fig. 1).4-6

FIGURE 1
View attachment 9235
Receptors controlling sebum production (adapted from Zhang et al.7).


Each of these newly identified receptors is activated by a dietary substance. The peroxisome proliferator‐activated receptors (PPARα, β and γ) are stimulated by free fatty acids and cholesterol, the insulin‐like growth factor (IGF)‐1 receptor by sugar and leptin receptor by fat.7-9 Leptin is a hormone secreted by adipocytes that regulates bodyweight and is also known to link lipid metabolism with inflammation in various cell types. In the sebocyte, it is responsible for creating lipid droplets within the cell and has recently been shown to induce pro‐inflammatory enzyme and cytokine (interleukin (IL)‐6 and IL‐8) secretion as well.9 This result suggests that leptin is a novel player in inducing inflammation and altering lipid profile in sebocytes and could be a link between diet and development of inflammatory acne.

The link between acne and diet is further supported by a recent case–control study of predictive factors for acne.10 Apart from the well‐known relationship between family history and acne, the investigators found that a high body mass index (BMI) was also a predictive factor for an increased risk of developing moderate to severe acne in adolescents and young adults. Furthermore, a population‐based study of acne and BMI in adolescents reported that overweight as well as obesity may be potentially associated with acne in girls aged 18 and 19 years,11 even though proofs are still lacking.






Dihydrotestosterone: Biochemistry, Physiology, and Clinical Implications of Elevated Blood Levels

Dihydrotestosterone: Biochemistry, Physiology, and Clinical Implications of Elevated Blood Levels


Skin
Skin possesses all of the requisite steroidogenic capabilities to ensure local homeostatic control of steroid hormones, suggesting an important paracrine role for T, DHT, and estradiol within the skin, the function of which is poorly understood (143). Likewise, skin contains metabolizing pathways (e.g., glucuronidation; sulphation) that inactivate DHT (144). Consequently, localized mechanisms in skin maintain concentrations of DHT that are not meaningfully influenced by circulating DHT levels, probably due to the fact that the DHT concentration gradient favors secretion into blood (143, 145). In men, androgen levels are highest in the scrotal skin followed by pubic skin and then thigh skin, a pattern paralleled by 5α-reductase and low 3α-reductase activity (and thus tissue DHT) (146). In women, skin DHT concentrations are highest in the labia majora and clitoris followed by pubic skin and then thigh skin (147).

Absorption of DHT (as is also true for T) across the skin is a passive process that follows Fick’s law (148, 149). Accordingly, concentrations of DHT in skin to which DHT has been applied are extremely high during the period when DHT is absorbed into the bloodstream. A single transdermal DHT product is available in a handful of countries, and it is this formulation that has been used in clinical trials. Studies of topical DHT in hypogonadal or eugonadal men have not reported adverse effects on skin aside from mild irritation due to the high alcohol content, despite its direct application and sustained supraphysiological levels of DHT for up to 24 months (51, 52, 54). These results are consistent with those from shorter-term transdermal DHT studies (60, 103).

Male human skin and hair express an abundance of SRD5A type I in sebaceous glands, hair follicles, sweat glands, and the epidermis, whereas SRD5A type II is expressed in genital keratinocytes and hair follicles (150). The physiologic role of DHT in the skin is unclear, but it is hypothesized that sex steroids may influence the immune function of skin and locally influence inflammatory processes (143). Androgens clearly play a role in the pathogenesis of acne vulgaris, likely through increased sebum production, and may impact cutaneous wound healing (151); however, a specific role for DHT in many of these processes has not been demonstrated. An exception to this may be DHT-induced upregulation of inflammatory cytokines (e.g., IL-1, IL-6, and tumor necrosis factor-α) in acne (152). Studies of agents that reduce levels of DHT in skin clearly support a role for DHT in the development of male androgenic alopecia (MAA) (male pattern baldness). This is inferred, in part, by the effectiveness of 5AR-Is in suppressing the progression of MAA and the observations that castrated men and men with SRD5A deficiency do not develop baldness (153). However, the effectiveness of SRD5A therapy likely resides at the level of the hair follicle (i.e., lowered follicular concentrations of DHT) and not a reduction of circulating DHT because this has not been shown to correlate with MAA. Support for this conclusion is also found in a study of men exposed to exceptionally high levels of DHT in response to daily application of a DHT gel preparation for 24 months. DHT was not associated with acne, MAA, or other androgen-associated skin pathology (54). Instead, the most important factor in the pathogenesis of MAA is a genetic predisposition for AR polymorphisms [e.g., synonymous nucleotide polymorphism in exon 1 (rs6152) of the AR] (154, 155). In addition, differences in AR concentrations and steroid-converting enzymes in the hair follicle also appear to be play a significant role in MAA (156).

Fantastic @madman . Thank you very much. Thats a great article.

I have noticed that even a slight increase in my total weekly dosage results in increased acne. So it is dose related from my POV.
(i used 100mg/week in my example as it was such a round number to explain my point)

I respond massively to exogenous testosterone. (my dad is the same)

60 mg /week (cypionate) using an EoD injection protocol puts my,
TT: 1000
E2: 30
SHBG:40

thats in the trough (if there is one on an EoD protocol) an hour before injection is due.

So the plan of adding in nandrolone decanoate would be to drop the cypionate to 50mg/week, and add 20mg nandrolone decanoate to the protocol.

i played around for a while with propionate (which i loved), however the acne was very bad.

Protocol was :
70mg/week (propionate) ED injection (10mg /day)
Bloodwork was mental tbh.
My daily deviation was massive.

TT:1100 (at 10.00, 2 hours after pin)
TT:350 (08:00 , 2 hours before pin)

I felt great though TBH. No PIP, no sides except the acne. I wish i had done a DHT reading as part of the blood panel.

 

[Cataceous]

...
Protocol was :
70mg/week (propionate) ED injection (10mg /day)
Bloodwork was mental tbh.
My daily deviation was massive.

TT:1100 (at 10.00, 2 hours after pin)
TT:350 (08:00 , 2 hours before pin)

I felt great though TBH. No PIP, no sides except the acne. I wish i had done a DHT reading as part of the blood panel.

Unrelated to current topic, but thanks for sharing this. I like seeing confirmation that my results with propionate are not unusual. You've got at least a 50% variation about the mean, which is similar to what I see, and is why I'm using a little enanthate with my propionate to damp down the variation a bit.

If I might ask: what exactly was your EOD cypionate dose? 17 mg? 20 mg? What I can't figure out is why your total testosterone on cypionate is so relatively high; it should almost represent the average of peak and trough for propionate, or lower due to the lower dose. Surely the propionate peak isn't so much higher than what you measured 2 hours post-injection?

 

[bp]

Unrelated to current topic, but thanks for sharing this. I like seeing confirmation that my results with propionate are not unusual. You've got at least a 50% variation about the mean, which is similar to what I see, and is why I'm using a little enanthate with my propionate to damp down the variation a bit.

If I might ask: what exactly was your EOD cypionate dose? 17 mg? 20 mg? What I can't figure out is why your total testosterone on cypionate is so relatively high; it should almost represent the average of peak and trough for propionate, or lower due to the lower dose. Surely the propionate peak isn't so much higher than what you measured 2 hours post-injection?

EoD cypionate (60mg weekly dose) 'testex prolongatum, desma pharmaceuticals."
17mg EoD

something else you might find of interest @Cataceous ,

Initially when starting TRT my protocol used bayer schering enanthate.

My initial dosage was far too high with a TT of 2530. (E3.5D protocol, with the bloodwork being done the day of injection, 2hrs after pinning)

I received the results within a day, and immediately stopped the protocol (to allow my body to 'purge' the excess testosterone)

8 days later i did new bloods.

TT of 320

Now im far from the worlds greatest mathematician. But that looks to me that 3 half lives took place over an 8 day period. Suggesting that for me, testosterone enanthate has a half life of around 2.5-3 days. Far shorter than medical text would have me believe.

 

[Cataceous]

...
Now im far from the worlds greatest mathematician. But that looks to me that 3 half lives took place over an 8 day period. Suggesting that for me, testosterone enanthate has a half life of around 2.5-3 days. Far shorter than medical text would have me believe.

Traditionally serum testosterone after an injection is modeled by bi-exponential behavior, with the rate of absorption yielding one constant of proportionality and the rate of use yielding the other. I've played around with a different model for absorption, in which the rate is governed by the surface area of the injected depot. What I like about your measurements is that they tend to preferentially support this model, which can match an appropriate exponential decay early on, but then lacks the long tail seen with exponentials. In other words, you might see a drop by half from the peak in about five days, but after that the drop is considerably faster.

 

[pfuked]

in my 30s I did nandrolone with low dose Test for prolonged periods of time--it grew back all the hair I was losing at the time. worked 10x better than minoxidil

Theoretically, this should work. Nandrolone produces DHN, which is like a weaker form of DHT. I’ve been talking to a lot of guys using nandrolone as their base, with small doses of test to boost E2 up a bit. I’m pretty sure all of them report less acne and bloating. A few of them have actually reported that the hair on their head got thicker. So if you’re having any issues due to high DHT or high E2, what you plan on doing should work quite well. You’re going to be lowering DHT and E2, while actually having slightly more androgen receptor activation than on 100mg of test. Nandrolone is 25% more anabolic than testosterone. So by using 70mg of test, and 30mg of nandrolone, you’ll have a slightly higher anabolic response, while slightly decreasing E2 and DHT. Theoretically I’d say this experiment should result in a win win.

 

[fifty]

Really?

 

[SilverSurfer]

in my 30s I did nandrolone with low dose Test for prolonged periods of time--it grew back all the hair I was losing at the time. worked 10x better than minoxidil

Seriously? How long were you taking it? Protocol?

Fortunately, I have a full head of hair, but I’m sure there are plenty of guys here who would be interested.

 

[bochinit]

And what about erectile dysfunction?

 

[Gman86]

in my 30s I did nandrolone with low dose Test for prolonged periods of time--it grew back all the hair I was losing at the time. worked 10x better than minoxidil

Ive actually heard stories about guys using nandrolone as their base, and their hair on their head actually getting thicker! Idk if it’s just because they don’t have high levels of DHT anymore, or if there’s a mechanism of nandrolone that specifically aids in hair growth on the scalp. I know nandrolone is a strong anti-inflammatory, which maybe has something to do with the hair regrowth.

 

[pfuked]

It was about 20 years ago. I cant remember the specifics but I don't think it was more than 200 mg deca a week with a small amout of test cyp. Probably like 50 mg a week of test cyp

No joke, it actually grew back my hair. Perhaps since my body wasn't producing as much DHT due to the low dose of test cyp. Also, since nandrolone conversion via 5 alpha-reductase to Dihydronandrolone is a weaker androgen receptor agonist compared to DHT, probably also played a big role...

 

[pfuked]

my erections were fine, and I didn't have to take an AI like I do now with my current regimen-- 60 mg test cyp with 100 units HCG every three days

I was doing the nandrolone with low dose testosterone continuously - as a replacement strategy I used at the time.

 

[Gman86]

my erections were fine, and I didn't have to take an AI like I do now with my current regimen-- 60 mg test cyp with 100 units HCG every three days

I was doing the nandrolone with low dose testosterone continuously - as a replacement strategy I used at the time.

Very interesting. My current protocol, as of yesterday is basically just what you were on 20 years ago. I’m currently on 200mg deca, 35mg test, and 500iu’s HCG.

What made you even consider using nandrolone as your base 20 years ago? And the fact that you knew to use low dose test, I’m assuming to boost e2, you were way ahead of your time with this way of thinking/ protocol.

So you’re currently only doing 100iu’s of HCG E3D? Why such a low dose?