Testosterone plus Nandrolone = Estrogen overload?

[tareload]

Does LDN increase cortisol?

Good question.

Here's where I would start but I don't know the definitive answer to your question or if there is one. It's a very general question.

Age-Dependent and Gender-Dependent Regulation of Hypothalamic-Adrenocorticotropic-Adrenal Axis

Naltrexone effects on cortisol secretion in women and men in relation to a family history of alcoholism: studies from the Oklahoma Family Health Patterns Project - PubMed

Naltrexone evokes a cortisol response through its blockade of central opioid receptors on the hypothalamic-pituitary-adrenocortical axis (HPA). The magnitude of this cortisol response may be useful as a probe for central opioid activity in different groups of subjects. Accordingly, the present...

pubmed.ncbi.nlm.nih.gov

Gender, age, dose, genes, etc, etc.

Hypothalamic-Pituitary-Adrenocortical (HPA) Axis Response and Biotransformation of Oral Naltrexone: Preliminary Examination of Relationship to Family History of Alcoholism - Neuropsychopharmacology

We examined HPA axis response to 50 mg oral naltrexone compared with placebo in 17 healthy male and female nonalcoholic subjects, approximately half of whom had a positive family history of alcoholism (FH+) and half of whom who did not (FH−). Mood response and naltrexone biotransformation were...

www.nature.com

 

[Gman86]

Good question.

Here's where I would start but I don't know the definitive answer to your question or if there is one. It's a very general question.

Age-Dependent and Gender-Dependent Regulation of Hypothalamic-Adrenocorticotropic-Adrenal Axis

View attachment 17777

Naltrexone effects on cortisol secretion in women and men in relation to a family history of alcoholism: studies from the Oklahoma Family Health Patterns Project - PubMed

Naltrexone evokes a cortisol response through its blockade of central opioid receptors on the hypothalamic-pituitary-adrenocortical axis (HPA). The magnitude of this cortisol response may be useful as a probe for central opioid activity in different groups of subjects. Accordingly, the present...

pubmed.ncbi.nlm.nih.gov

View attachment 17776


Gender, age, dose, genes, etc, etc.

Hypothalamic-Pituitary-Adrenocortical (HPA) Axis Response and Biotransformation of Oral Naltrexone: Preliminary Examination of Relationship to Family History of Alcoholism - Neuropsychopharmacology

We examined HPA axis response to 50 mg oral naltrexone compared with placebo in 17 healthy male and female nonalcoholic subjects, approximately half of whom had a positive family history of alcoholism (FH+) and half of whom who did not (FH−). Mood response and naltrexone biotransformation were...

www.nature.com

I was basically jw if it was a corticosteroid like prednisone or hydrocortisone. So it acts on the opioid receptors?

 

[tareload]

I was basically jw if it was a corticosteroid like prednisone or hydrocortisone. So it acts on the opioid receptors?

Yes. Opioid receptor antagonist.

 

[DS3]

Noticeable after 4-6 weeks on and really kicked in after week 10. We don't really know how long the metabolites of ND stick around (a good while) but after 3 months off I noticed a difference and 9 months later I was pretty much back to my critical, manageably depressed norm .

For the record, LDN brings on these symptoms for me much quicker (within a week or two).

Same experience here with nandrolone.

 

[equel]

ments the androgenic base of testosterone by supplementing additional anabolic activity without strong estrogenicity. The resulting stack is almost as productive as a cycle utilizing a higher dose of testosterone alone but less problematic in terms of estrogenic side effects such as water retention, gynecomastia, and fat buildup.

What the actual fuck am I even reading? Dude, you clearly have zero experience with steroids, jesus christ you are so misinformed and so much of the stuff u write on this board is redicilous.

 

[equel]

Really.....LMFAO!

You might wanna look up who William Llewellyn is.

Lol @ still refering to William, this guys theories have been debunked (many of them) a long time ago. Get with the program grandpa.

 

[equel]

Madman you ever tried a 100/100 split of test/ND or something similar? Any personal antidote?

I like how the gym feels and the way I look on 200mg of T but everything else sucks. I know it's cheesy but I'm just being real. Seems like a 100/100 split may be a good way to go and make my joints feel good too.

Also what is the decanoate ester half life? I've read 1 week but also have read 2 weeks

I suggest you do not follow madmans advice, ive read alot of his shit recently and he is very very misinformed when it comes to things.

 

[equel]

I have to agree, Taeian is an idiot.

Plenty threads on plenty pro BB boards with the reasonings of seasoned BBers, many of which have tried such things.

If you want your pecker to permanently fail, just experiment with one of his ND only cycles. See what happens AFTER the cycle.

Done it for a long time now, deca/npp only = awesome libido, gains everything. Its the best shit ive ever done for myself.

 

[equel]

Nandrolone increasing prolactin is incorrect. Nandrolone converts extremely little into E2 and prolactin. It’s an old old myth that nandrolone shoots up prolactin levels. However, as far as I know it does sensitive E2 and prolactin receptors, so whatever E2 and prolactin u have in ur system can become more “potent”. That’s why caution is required when concurrently using a compound that has a high conversion rate to both E2 and prolactin, like testosterone, for example

Correct. In studies testosterone increase prolactin, nandrolone decrease it (if ran solo).

 

[equel]

19-Nors cause an increase in prolactin. They do not convert to prolactin. This is a well known fact in BB circles and why caber is used in cycles containing 19-Nor compounds. This has been found from the blood results of thousands on bodybuilders.

Perhaps this applies to bodybuilding doses and may not apply to say 50mg/week.

False again. I dont give a fuck about "bb community", LOOK at the studies. Every study ever done on nandrolone = decrease prolactin.
Caber is used because they combine it with test. Nand + test = huge prolactin spike.

 

[equel]

On the contrary, deca DOES cause an increase in prolactin (which is totally different from CONVERTING to prolactin, a concept you appear to have trouble grasping). Suggest you use the search function on a couple BB forums and you will find 1000s of results showing otherwise. Sure, these may be large doses, but the point needs to be made.

No, it does NOT increase prolactin. Jesus christ. BB FORUMS = THEY USE IT WITH TEST; do u understand? The nand + test = increase in prolactin, NOT nand only.

I wish that so many of you could just shut ur mouth til u get actual experience, sigh.

 

[Gman86]

Done it for a long time now, deca/npp only = awesome libido, gains everything. Its the best shit ive ever done for myself.

Do u run run deca/ npp by itself indefinitely, or do u cycle it for certain periods of time?

 

[bixt]

Actually looking forward to @madmans reply

I think excelmale is the last remaining forum/group the troll @equal hasnt been banned (yet) from

 

[tareload]

Actually looking forward to @madmans reply

I think excelmale is the last remaining forum/group the troll @equal hasnt been banned (yet) from

Haha, only very slightly related, I'm not a troll but I have been banned from TNation now. Sometimes it may not be a bad thing.

@equel is doing better than me; he's not banned from T Nation .

 

[tareload]

Done it for a long time now, deca/npp only = awesome libido, gains everything. Its the best shit ive ever done for myself.

It's Amazing How Even Moderate Dose T Ruins My Libido/Boners

Been talking bout this before, but figured ima say it again as its been a while: Tried upping from 10mg test ED to 100mg a week (Yes once a week, Ive tried splitting em etc, dont matter at that dosage for me). 10mg ED gives me ok/decent libido and erections. 100mg a week? GONE, libido ZERO...

forums.t-nation.com

Excerpt from this post:

Tried upping from 10mg test ED to 100mg a week (Yes once a week, Ive tried splitting em etc, dont matter at that dosage for me).

10mg ED gives me ok/decent libido and erections.

100mg a week? GONE, libido ZERO boner ZERO, nada, zipppp.

Alright, so decided to do an NPP (only) blast again.

Waited 11-14 days after my last 100mg injection.

Started injecting 300mg NPP 3 days ago (will do 3times a week AKA 900mg a week).

END Excerpt

Some of your previous comments I've agreed with (aka 10 mg/day of TC, very conservative dose Test to avoid E2 issues or AI). But come on man, 900 mg/week of ND or running ND solo? You aren't really suggesting that would be a viable TRT or even TOT protocol, are you? Just wanted to check (my heart is in pain from thinking about that).

Bias disclaimer: I have a fondness for you given our shared dislike for Danny Bossa's (at least past) reasoning and advice.

 

[Cataceous]

Haha, only very slightly related, I'm not a troll but I have been banned from TNation now. Sometimes it may not be a bad thing.
...

I had to go over there and read your last stand. Heroic. Makes them look pathetic and paranoid. Of course I promote the same views over here with even less equivocation.

...@equel is doing better than me; he's not banned from T Nation .

Maybe we could persuade him to hang out there exclusively. Condescension and personal attacks are an unwelcome addition to this forum.

 

[tareload]

I had to go over there and read your last stand. Heroic. Makes them look pathetic and paranoid. Of course I promote the same views over here with even less equivocation.

I appreciate it Sir. For those that need some light bedtime reading. In reverse chronological order:

Lost All My Gains During PCT

You started PCT too early. The standard bro knowledge of 2 weeks in between last jab and PCT is BS. Research test stasis/taper if you want to cycle successfully. Otherwise its blast and cruise, which if you want children, is a no go. SB

forums.t-nation.com

There Are No Safe Methods For Recreational AAS Use

EDIT: Moderator edited my thread title but here’s what it was designed to read… Pharma Forum Description is Incorrect: There Are No Safe Methods For Recreational AAS Use Here you go. Just in case you are new here, read the Pharma forum description (copied above), and think you are going to...

forums.t-nation.com

Edit the Description for the Pharma Forum

I’d propose changing the last sentence under the Pharma section description to: This forum is intended for the discussion of effective and least harm methods of using anabolics and managing post-cycle therapy (PCT). There are no safe methods for AAS abuse and the current phrasing above gives...

forums.t-nation.com

I think what finally sealed the deal was this article they published where what CT mentioned was exactly what I was arguing:

T Nation Content

Discover a more intelligent approach for getting bigger, stronger, and leaner.

www.t-nation.com

I tried to comment on the article (Colucci must moderate the comments too) and told Colucci to get with CT and get some consistency on the site. I don't think he liked that very much.

 

[madman]

What the actual fuck am I even reading? Dude, you clearly have zero experience with steroids, jesus christ you are so misinformed and so much of the stuff u write on this board is redicilous.

My reply is in post #6.

Must have gone over your head!

Common f**king sense that nandrolone is less prone to causing cosmetic sides especially when using therapeutic doses.

You that so-called bodybuilder from Sweden.....LMFAO!

 

[bixt]

Bias disclaimer: I have a fondness for you given our shared dislike for Danny Bossa's (at least past) reasoning and advice.

Went into Danny's circle with an open mind and now have an immense dislike for the guy. But if there was one thing which was true...it was his criticism of @equals methodology. @equal refuses to stick to a protocol and wait a couple months. If no immediate results are obtained, the protocol is deemed shit. Let me illustrate:

From @equals post on T-nation:

" Started injecting 300mg NPP 3 days ago (will do 3times a week AKA 900mg a week).

Today, waking up with the biggest boner on earth, extremely horny and cock just refuse to lay down."

That post was dated 15 DAYS ago, and he believes he now believes he has found the solution for his dick problems. Its too soon dude! You are in some kind of 900mg NPP dopamine induced honeymoon. How about you 1. run your "protocol" for many months first to see if it sticks and 2. check your health parameters after that to assess other health markers.

Heres another gem : " Steroids start working immidately as you inject them. Why u think scientists do studies where they give a rat, man, or whatever, a test shot to then observe the behavioral changes? That would make no sense if it would take several weeks for it to “work”. It works IMMIDATELY"

 

[madman]

False again. I dont give a fuck about "bb community", LOOK at the studies. Every study ever done on nandrolone = decrease prolactin.
Caber is used because they combine it with test. Nand + test = huge prolactin spike.

Might want to renege on that one!

*In all five volunteers levels of LH, FSH, and testosterone were reduced throughout treatment; prolactin levels were unchanged (fig 2).




REVERSIBLE AZOOSPERMIA INDUCED BY THE ANABOLIC STEROID 19-NORTESTOSTERONE (1984)

Subjects and Methods

Five healthy men aged 21-25 years consented to participate in the study after receiving extensive information about its aims and risks, in accordance with German drug regulations. None of the subjects had ever had any serious disease. All were active in sports and, aware that they were receiving an anabolic steroid, undertook heavy physical training during the treatment phase. The subjects had stable sexual relations during the investigation.

Physical examination, clinical chemistry, hematology, serum levels of the hormones luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin, and testosterone, and semen analysis (sperm density, motility, morphology, and seminal fructose) were carried out twice during the control period (A and B): all results were normal. All subjects’ spermatozoa were functionally intact as assessed in the heterologous ovum penetration test.8,9

The subjects were given intramuscular. injections of 19- nortestosterone-hexoxyphenylpropionate (Pharmaleo, Ratingen, West Germany), for the first 3 weeks 100 mg per week, then two 100 mg injections per week for a further 10 weeks. Throughout the study, the subjects were examined physically, and body weight and testicle and prostate size (as assessed by orchidometer and rectal palpation, respectively) were recorded. Blood samples for endocrine measurements were taken at the end of every week before administration of the next dose, as well as 1, 4, 8, 16, and 20 weeks after the last injection. Clinical chemistry was repeated in weeks 2, 5, 8, and 11 of treatment and 1, 4, 8, 12, 16, and 20 weeks after treatment. Ejaculates were obtained during weeks 4, 7, 11, 12, and 13 of treatment. All subjects were followed up for 16 weeks. Seminal parameters had then returned to normal in two subjects. The remaining three were followed up to week 24.

Semen evaluation was carried out according to World Health Organisation guidelines. 10 The subjects were requested to abstain from sexual activity for 48 h-7 days before the investigation (48 h in most cases). Testosterone was isolated from serum and separated from 19-nortestosterone by high-performance liquid chromatography, then measured by radioimmunoassay. 1,12 Reagents s provided by the WHO Matched Reagents Programme were used for measurement of serum LH by radioimmunoassay. FSH (IRE, Dusseldorf, West Germany) and prolactin (Serono, Freiburg, West Germany) were measured with commercially available radioimmunoassay kits.

All results, expressed as mean±SEM, were analyzed by Student’s s paired t-test with the means of the two control values (A and B) as points of reference.




Results

None of the five volunteers complained of any discomfort during the study and there were no effects on general health, no gynecomastia, and no acne. Prostate size did not change. Libido and potency as reported in weekly interviews were unaltered. Testicular volumes fell from 39±3 ml to 21±3 ml at the end of treatment but returned to the original volume 16 weeks after treatment (fig 1). Bodyweight (87.5±0.9 kg at the beginning of the study) increased continuously to 94.0±1.9 kg at the end of treatment; 16 weeks after treatment it had fallen to 92.0±2.6 kg.

In all five volunteers levels of LH, FSH, and testosterone were reduced throughout treatment; prolactin levels were unchanged (fig 2). FSH and LH remained below control levels until 8 and 16 weeks after treatment, respectively, and FSH was significantly above the control level at week 16. Serum testosterone concentrations returned to normal even more slowly, reaching control levels 6 months after the last injection.

Azoospermia was first observed in one subject after 7 weeks’ treatment, and by week 13 all five men were azoospermic (fig 3). Azoospermia persisted for 4 to 14 weeks after treatment. However, the volunteer who first became azoospermic had 0 - 2 million sperm per ml in the first post-treatment week. Seminal measurements had returned to normal 8 weeks after treatment in one subject, 14 weeks in another, and 20 weeks in two. In the fifth subject, recovery was slow; 24 weeks after treatment the sperm concentration was still only 1 million/ml. (However, when subject 5 was investigated 30 weeks after treatment, all his seminal parameters had returned to normal: 33 million sperm/ml, 75% motile sperm, 51% normally formed sperm.) Whenever the heterologous ovum penetration test could be done the sperm were classified as functionally normal, except in subject 5 after 11 weeks’ treatment, when only 3% of the hamster eggs were penetrated (lower normal limit 10%). Ejaculate volumes and seminal fructose concentrations did not change significantly during the study (fig 1).

Serum levels of alanine and aspartate aminotransferases and lactate dehydrogenase were significantly raised on one or two occasions, whereas y-glutamyl transpeptidase, alkaline phosphatase, and bilirubin did not rise above control levels (see table). Creatinine was raised on four occasions, but uric acid, cholesterol, and protein did not change significantly. The reticulocyte count slowly increased and reached peak values 4 weeks after the last injection: the highest erythrocyte count, hemoglobin, and hematocrit values occurred in weeks 8 and 12.



Discussion

19-nortestosterone is one of the most widely used anabolic steroids, both in clinical medicine and in athletics. It is surprising that this well-known steroid, which has been used for more than 20 years without reports of serious toxic side-effects, has these drastic effects on spermatogenesis. Possible explanations are that cachectic or convalescent patients receiving this steroid are not likely to be primarily interested in reproduction and that the testicular function of athletes taking the steroids secretly has never been thoroughly investigated. The dosage we tested is somewhat higher than that usually given to patients (50 mg/month to 100 mg/week) but is still lower than the quantities occasionally injected by athletes on the assumption that the drug will improve performance in competition.

After 7-12 weeks’ treatment up to 4-14 weeks after the end of treatment the subjects could be considered infertile. The periods of azoospermia lasted for 5-20 weeks if the sperm concentration of 0 • 2 million/ml in one subject in the first post-treatment week is disregarded. The suppression of spermatogenesis is apparently caused by suppression of pituitary gonadotropins secretion. In contrast to Bijlsma et al,13 who described a fall in FSH and testosterone but not LH with 19-nortestosterone, we found simultaneous falls in LH, FSH, and testosterone.

Despite reduced testosterone levels none of our subjects reported a loss of libido or potency. This observation, together with the fact that prostate size, ejaculate volume, and seminal fructose levels did not change, indicates that 19-nortestosterone given in such doses has sufficiently high androgenic potency. In contrast, neither prostate hypertrophy nor acne, which would be expected with a similar testosterone dosage, developed. Therefore, the androgenic properties of 19-nortestosterone seem to be lower than those of testosterone. 19-nortestosterone itself does not bind to estrogen receptors14 and is poorly converted to estrogens. These facts may account for the lack of acne and gynecomastia in our subjects.

The long-lasting suppression of serum LH, FSH, and testosterone after treatment indicates that 19-nortestosterone must remain in the body for some time. This finding may also explain why recovery of seminal parameters, at least in one subject, was very slow. However; the observation of an extended recovery phase is not uncommon in clinical trials of male fertility control based on steroid treatment. 1 5

Testicular size decreased by 50% under treatment, lagging behind the fall in sperm count. None of the subjects nor their sexual partners noticed the reduction in testicular size and none was informed about it to avoid psychological complications. This unrecognized effect cannot be considered an impeding side-effect.

The erythropoietic effect seen at the end of the treatment phase was expected since androgens and especially their 5(3-metabolites stimulate erythropoiesis.16,17 17-methyl-19- nortestosteronel8 and 17 -ethyl-19-nortestosteroneI9 9 are hepatotoxic, owing to 17-alkylation, but such effects have not been reported for 19-nortestosterone. The increase in aminotransferase levels may be of muscular rather than hepatic origin since the volunteers took heavy physical exercise during treatment and y-glutamyl transpeptidase, alkaline phosphatase, and bilirubin levels did not increase. The gain in body weight was apparently due to the muscular exercise rather than to an anabolic effect of 19-nortestosterone, since in normal men physical exercise increases muscle mass, regardless of whether an anabolic steroid has been administered.6,7

Testosterone or progestagens given as single entities fail to give effective and acceptable male fertility control;4,5,20 however, the combination of testosterone with progestagens or danazol appears more favorable.21,22 19-nortestosterone, an effective androgen-but approximately ten times more progestagenic than testosterone,14 has the qualities of -an androgen and a progestagen in a single molecule. Difficulties resulting from the different pharmacokinetics of two steroids given in combination and mutual interference are avoided when 19-nortestosterone is given alone. The effectiveness of 19-nortestosterone in suppressing spermatogenesis and simultaneously maintaining androgenic effects, as well as the long history of this drug uneventful in terms of toxic side-effects, render it an interesting candidate for further evaluation as an agent for male fertility control.