Nandrolone Experiences

madman

Member
studies agree with me. So no I won't speak for myself lol, I seldom do when i make a claim it's what data say.

But yeah high dose test will blow you up like a water buffalo. I like my gains lean, my prostate small, and my hair juvenile! Couldn't care less about strength gains, I don't need to bench XYZ pounds to feel alpha.



perhaps. I was talking about "insulin independent glucose transport", might wanna google that one?

William Llewellyn’s, ANABOLICS


Estrogen Aromatization

Testosterone is the primary substrate used in the male body for the synthesis of estrogen (estradiol), the principal female sex hormone. Although the presence of estrogen may seem quite unusual in men, it is structurally very similar to testosterone. With a slight alteration by the enzyme aromatase, estrogen is produced in the male body. Aromatase activity occurs in various regions of the male body, including adipose,22 liver,23 gonadal,24 central nervous system,25, and skeletal muscle 26 tissues. In the context of the average healthy male, the amount of estrogen produced is generally not very significant to one's body disposition, and may even be beneficial in terms of cholesterol values (See Side Effects: Cardiovascular System). However, in larger amounts, it does have the potential to cause many unwanted effects including water retention, female breast tissue development (gynecomastia), and body fat accumulation. For these reasons, many focus on minimizing the build-up or activity of estrogen in the body with aromatase inhibitors such as Arimidex and Cytadren, or antiestrogens such as Clomid or Nolvadex, particularly at times when gynecomastia is a worry or the athlete is attempting to increase muscle definition.

We must, however, not be led into thinking that estrogen serves no benefit. It is actually a desirable hormone in many regards. Athletes have known for years that estrogenic steroids are the best mass builders, but it is only recently that we are finally coming to understand the underlying mechanisms why. It appears that reasons go beyond the simple size, weight, and strength increases that one would attribute to estrogen-related water retention, with this hormone actually having a direct effect on the process of anabolism. This is manifest through increases in glucose utilization, growth hormone secretion, and androgen receptor proliferation.

Glucose Utilization and Estrogen

Estrogen may play a very important role in the promotion of an anabolic state by affecting glucose utilization in muscle tissue. This occurs via altering of the level of available glucose 6-phosphate dehydrogenase, an enzyme directly tied to the use of glucose for muscle tissue growth and recuperation.27 28 More specifically, G6PD is a vital part of the pentose phosphate pathway, which is integral in determining the rate nucleic acids and lipids are to be synthesized in cells for tissue repair. During the period of regeneration after skeletal muscle damage, levels of G6PD are shown to rise dramatically, which is believed to represent a mechanism for the body to enhance recovery when needed. Surprisingly, we find that estrogen is directly tied to the level of G6PD that is to be made available to cells in this recovery window.

The link between estrogen and G6PD was established in a study demonstrating levels of this dehydrogenase enzyme to rise after the administration of testosterone propionate. The investigation further showed that the aromatization of testosterone to estradiol was directly responsible for this increase, and not the androgenic action of this steroid.29 The non-aromatizable steroids dihydrotestosterone and fluoxymesterone were tested alongside testosterone propionate but failed to duplicate the effect of testosterone. Furthermore, the positive effect of testosterone propionate was blocked when the aromatase inhibitor 4- hydroxyandrostenedione (formestane) was added, while 17-beta estradiol administration alone caused a similar increase in G6PD to testosterone propionate. The inactive estrogen isomer alpha estradiol, which is unable to bind the estrogen receptor, failed to do anything. Further tests using testosterone propionate and the anti-androgen flutamide showed that this drug also did nothing to block the positive action of testosterone, establishing it as an effect independent of the androgen receptor.


Estrogen and GH/IGF-1

Estrogen may also play an important role in the production of growth hormone and IGF-1. IGF-1 (insulin-like growth factor) is an anabolic hormone released in the liver and various peripheral tissues via the stimulus of growth hormone (See Drug Profiles: Growth Hormone). IGF-1 is responsible for the anabolic activity of growth hormones such as increased nitrogen retention/protein synthesis and cell hyperplasia (proliferation). One of the first studies to bring this issue to our attention looked at the effects of the anti-estrogen tamoxifen on IGF-1 levels, demonstrating it to have a suppressive effect.30 A second, perhaps more noteworthy, the study took place in 1993, which looked at the effects of testosterone replacement therapy on GH and IGF-1 levels alone, and compared them to the effects of testosterone combined again with tamoxifen.31 When tamoxifen was given, GH and IGF-1 levels were notably suppressed, while both values were elevated with the administration of testosterone enanthate alone. Another study has shown 300 mg of testosterone enanthate weekly to cause a slight IGF-1 increase in normal men. Here the 300 mg of testosterone ester caused an elevation of estradiol levels, which would be expected at such a dose. This was compared to the effect of the same dosage of nandrolone decanoate; however, this steroid failed to produce the same increase. This result is quite interesting, especially when we note that estrogen levels were actually lowered 32 when this steroid was given. Yet another demonstrated that GH and IGF-1 secretion is increased with testosterone administration on males with delayed puberty, while dihydrotestosterone (non-aromatizable) seems to suppress GH and IGF-1 secretion.


Estrogen and the Androgen Receptor

It has also been demonstrated that estrogen can increase the concentration of androgen receptors in certain tissues. This was shown in studies with rats, which looked at the effects of estrogen on cellular androgen receptors in animals that underwent orchiectomy (removal of testes, often done to diminish endogenous androgen production). According to the study, administration of estrogen resulted in a striking 480% increase in methyltrienolone (a potent oral androgen often used to reference receptor binding in studies) binding in the levator ani muscle.34 The suggested explanation is that estrogen must either be directly stimulating androgen receptor production or perhaps diminishing the rate of receptor breakdown. Although the growth of the levator ani muscle is commonly used as a reference for the anabolic activity of steroid compounds, it is admittedly a sex organ muscle, and different from skeletal muscle tissue in that it possesses a much higher concentration of androgen receptors. This study, however, did look at the effect of estrogen in fast-twitch skeletal muscle tissues (tibialis anterior and extensor digitorum longus) as well but did not note the same increase as the levator ani. Although discouraging at first glance, the fact that estrogen can increase androgen receptor binding in any tissue remains an extremely significant finding, especially in light of the fact that we now know androgens to have some positive effects on muscle growth that are mediated outside of muscle tissue.


Estrogen and Fatigue

“Steroid Fatigue” is a common catchphrase these days, and refers to another important function of estrogen in both the male and female body, namely its ability to promote wakefulness and a mentally alert state. Given the common availability of potent third-generation aromatase inhibitors, bodybuilders today are (at times) noticing more extreme estrogen suppression than they had in the past. Often associated with this suppression is fatigue. Under such conditions, the athlete, though on a productive cycle of drugs, may not be able to maximize his or her gains due to an inability to train at full vigor. This effect is sometimes also dubbed “steroid lethargy.” The reason is that estrogen plays an important supporting role in the activity of serotonin. Serotonin is one of the body's principal neurotransmitters, vital to mental alertness and the sleep/wake cycle.35 36 Interference with this neurotransmitter is also associated with chronic fatigue syndrome,37 38 so we can see how vital it is to fatigue specifically. Estrogen suppression in menopause has also been associated with fatigue,39 as has the clinical use of newer (more potent) aromatase inhibitors like anastrozole,40 letrozoles,41 exemestane,42 and fadrozole 43 in some patients. These things may be important to consider when planning your next cycle. Although not everyone notices this problem when estrogen is low, for those that do, a little testosterone or estrogen can go a long way in correcting this. It is also of note that the use of strictly non-aromatizable steroids sometimes causes this effect as well, likely due to the suppression of natural testosterone production (cutting off the main substrate used by the male body to make estrogen).

Anti-Estrogens and the Athlete

So what does this all mean to the bodybuilder looking to gain optimal size? Basically I think it calls for a cautious approach to the use of estrogen maintenance drugs if mass is the key objective (things change, of course, if we are talking about cutting). Obviously, antiestrogens should be used if there is a clear need for them due to the onset of estrogenic side effects, or at the very least, the drugs being administered should be substituted for non-estrogenic compounds. Gynecomastia is certainly an unwanted problem for the steroid user, as are noticeable fat mass gains. But if these problems have not presented themselves, the added estrogen due to a cycle of testosterone or Dianabol, for example, might indeed be aiding in the buildup of muscle mass or keeping you energetic. An individual confident they will notice or are not prone to getting, estrogenic side effects, may, therefore, want to hold off using estrogen maintenance drugs so as to achieve the maximum possible gains in tissue mass.


@Nelson Vergel:
Screenshot (1664).png

Screenshot (1665).png
 
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madman

Member



Growth hormone-insulin-like growth factor-1 axis


Men with congenital aromatase deficiency have impaired stimulated growth hormone (GH) secretion and low insulin-like growth factor-1 (IGF-1) (66).
Exogenous E2 in these men was not able to normalize GH secretion (66), possibly because of abnormal development of the GH–IGF-1 axis in the setting of congenital E2 deficiency or because restoration of normal circulating E2 concentration is insufficient if local E2 production remains impaired (67). Additional lines of evidence from preclinical models, women, and indirect evidence from men, suggest that E2 is important in regulation of GH secretion by both direct and indirect mechanisms (67, 68).


*In summary, E2 rather than testosterone appears the main sex steroid regulator of the GH-IGF-1 axis in men.
 

readalot

Member
William Llewellyn’s, ANABOLICS


Estrogen Aromatization

Testosterone is the primary substrate used in the male body for the synthesis of estrogen (estradiol), the principal female sex hormone. Although the presence of estrogen may seem quite unusual in men, it is structurally very similar to testosterone. With a slight alteration by the enzyme aromatase, estrogen is produced in the male body. Aromatase activity occurs in various regions of the male body, including adipose,22 liver,23 gonadal,24 central nervous system,25, and skeletal muscle 26 tissues. In the context of the average healthy male, the amount of estrogen produced is generally not very significant to one's body disposition, and may even be beneficial in terms of cholesterol values (See Side Effects: Cardiovascular System). However, in larger amounts, it does have the potential to cause many unwanted effects including water retention, female breast tissue development (gynecomastia), and body fat accumulation. For these reasons, many focus on minimizing the build-up or activity of estrogen in the body with aromatase inhibitors such as Arimidex and Cytadren, or antiestrogens such as Clomid or Nolvadex, particularly at times when gynecomastia is a worry or the athlete is attempting to increase muscle definition.

We must, however, not be led into thinking that estrogen serves no benefit. It is actually a desirable hormone in many regards. Athletes have known for years that estrogenic steroids are the best mass builders, but it is only recently that we are finally coming to understand the underlying mechanisms why. It appears that reasons go beyond the simple size, weight, and strength increases that one would attribute to estrogen-related water retention, with this hormone actually having a direct effect on the process of anabolism. This is manifest through increases in glucose utilization, growth hormone secretion, and androgen receptor proliferation.

Glucose Utilization and Estrogen

Estrogen may play a very important role in the promotion of an anabolic state by affecting glucose utilization in muscle tissue. This occurs via altering of the level of available glucose 6-phosphate dehydrogenase, an enzyme directly tied to the use of glucose for muscle tissue growth and recuperation.27 28 More specifically, G6PD is a vital part of the pentose phosphate pathway, which is integral in determining the rate nucleic acids and lipids are to be synthesized in cells for tissue repair. During the period of regeneration after skeletal muscle damage, levels of G6PD are shown to rise dramatically, which is believed to represent a mechanism for the body to enhance recovery when needed. Surprisingly, we find that estrogen is directly tied to the level of G6PD that is to be made available to cells in this recovery window.

The link between estrogen and G6PD was established in a study demonstrating levels of this dehydrogenase enzyme to rise after the administration of testosterone propionate. The investigation further showed that the aromatization of testosterone to estradiol was directly responsible for this increase, and not the androgenic action of this steroid.29 The non-aromatizable steroids dihydrotestosterone and fluoxymesterone were tested alongside testosterone propionate but failed to duplicate the effect of testosterone. Furthermore, the positive effect of testosterone propionate was blocked when the aromatase inhibitor 4- hydroxyandrostenedione (formestane) was added, while 17-beta estradiol administration alone caused a similar increase in G6PD to testosterone propionate. The inactive estrogen isomer alpha estradiol, which is unable to bind the estrogen receptor, failed to do anything. Further tests using testosterone propionate and the anti-androgen flutamide showed that this drug also did nothing to block the positive action of testosterone, establishing it as an effect independent of the androgen receptor.


Estrogen and GH/IGF-1

Estrogen may also play an important role in the production of growth hormone and IGF-1. IGF-1 (insulin-like growth factor) is an anabolic hormone released in the liver and various peripheral tissues via the stimulus of growth hormone (See Drug Profiles: Growth Hormone). IGF-1 is responsible for the anabolic activity of growth hormones such as increased nitrogen retention/protein synthesis and cell hyperplasia (proliferation). One of the first studies to bring this issue to our attention looked at the effects of the anti-estrogen tamoxifen on IGF-1 levels, demonstrating it to have a suppressive effect.30 A second, perhaps more noteworthy, the study took place in 1993, which looked at the effects of testosterone replacement therapy on GH and IGF-1 levels alone, and compared them to the effects of testosterone combined again with tamoxifen.31 When tamoxifen was given, GH and IGF-1 levels were notably suppressed, while both values were elevated with the administration of testosterone enanthate alone. Another study has shown 300 mg of testosterone enanthate weekly to cause a slight IGF-1 increase in normal men. Here the 300 mg of testosterone ester caused an elevation of estradiol levels, which would be expected at such a dose. This was compared to the effect of the same dosage of nandrolone decanoate; however, this steroid failed to produce the same increase. This result is quite interesting, especially when we note that estrogen levels were actually lowered 32 when this steroid was given. Yet another demonstrated that GH and IGF-1 secretion is increased with testosterone administration on males with delayed puberty, while dihydrotestosterone (non-aromatizable) seems to suppress GH and IGF-1 secretion.


Estrogen and the Androgen Receptor

It has also been demonstrated that estrogen can increase the concentration of androgen receptors in certain tissues. This was shown in studies with rats, which looked at the effects of estrogen on cellular androgen receptors in animals that underwent orchiectomy (removal of testes, often done to diminish endogenous androgen production). According to the study, administration of estrogen resulted in a striking 480% increase in methyltrienolone (a potent oral androgen often used to reference receptor binding in studies) binding in the levator ani muscle.34 The suggested explanation is that estrogen must either be directly stimulating androgen receptor production or perhaps diminishing the rate of receptor breakdown. Although the growth of the levator ani muscle is commonly used as a reference for the anabolic activity of steroid compounds, it is admittedly a sex organ muscle, and different from skeletal muscle tissue in that it possesses a much higher concentration of androgen receptors. This study, however, did look at the effect of estrogen in fast-twitch skeletal muscle tissues (tibialis anterior and extensor digitorum longus) as well but did not note the same increase as the levator ani. Although discouraging at first glance, the fact that estrogen can increase androgen receptor binding in any tissue remains an extremely significant finding, especially in light of the fact that we now know androgens to have some positive effects on muscle growth that are mediated outside of muscle tissue.


Estrogen and Fatigue

“Steroid Fatigue” is a common catchphrase these days, and refers to another important function of estrogen in both the male and female body, namely its ability to promote wakefulness and a mentally alert state. Given the common availability of potent third-generation aromatase inhibitors, bodybuilders today are (at times) noticing more extreme estrogen suppression than they had in the past. Often associated with this suppression is fatigue. Under such conditions, the athlete, though on a productive cycle of drugs, may not be able to maximize his or her gains due to an inability to train at full vigor. This effect is sometimes also dubbed “steroid lethargy.” The reason is that estrogen plays an important supporting role in the activity of serotonin. Serotonin is one of the body's principal neurotransmitters, vital to mental alertness and the sleep/wake cycle.35 36 Interference with this neurotransmitter is also associated with chronic fatigue syndrome,37 38 so we can see how vital it is to fatigue specifically. Estrogen suppression in menopause has also been associated with fatigue,39 as has the clinical use of newer (more potent) aromatase inhibitors like anastrozole,40 letrozoles,41 exemestane,42 and fadrozole 43 in some patients. These things may be important to consider when planning your next cycle. Although not everyone notices this problem when estrogen is low, for those that do, a little testosterone or estrogen can go a long way in correcting this. It is also of note that the use of strictly non-aromatizable steroids sometimes causes this effect as well, likely due to the suppression of natural testosterone production (cutting off the main substrate used by the male body to make estrogen).

Anti-Estrogens and the Athlete

So what does this all mean to the bodybuilder looking to gain optimal size? Basically I think it calls for a cautious approach to the use of estrogen maintenance drugs if mass is the key objective (things change, of course, if we are talking about cutting). Obviously, antiestrogens should be used if there is a clear need for them due to the onset of estrogenic side effects, or at the very least, the drugs being administered should be substituted for non-estrogenic compounds. Gynecomastia is certainly an unwanted problem for the steroid user, as are noticeable fat mass gains. But if these problems have not presented themselves, the added estrogen due to a cycle of testosterone or Dianabol, for example, might indeed be aiding in the buildup of muscle mass or keeping you energetic. An individual confident they will notice or are not prone to getting, estrogenic side effects, may, therefore, want to hold off using estrogen maintenance drugs so as to achieve the maximum possible gains in tissue mass.


@Nelson Vergel: View attachment 10149
View attachment 10150
Steer and heifer approved:

Liveweight Gains, Blood Levels of Metabolites, Proteins and Hormones Following Implantation of Anabolic Agents in Steers

SUMMARY
Eleven steers aged 12-14 months were divided into groups of three based on age, breed and liveweight. One animal in each group was implanted with trenbolone acetate, another with trenbolone acetate + oestradiol-17β, and the third animal served as control. The mean liveweight gains throughout a 9 week period were 54.3 kg, 64.3 kg and 77.2 kg for control, trenbolone acetate and trenbolone acetate + oestradiol treated groups respectively. The mean values for weight gains of the treated animals were significantly higher (P < 0.05) than the control values. The improvement in feed conversion in the treated animals was significant (P < 0.001) in the animals receiving trenbolone acetate + oestradiol.
No changes were seen in the plasma concentrations of growth hormone, prolactin and insulin. There was, however, a significant decrease in the concentration of total thyroxine in the plasma of the treated animals. The decrease was greatest in steers implanted with trenbolone acetate + oestra- diol-17β. The levels of serum urea and albumin were decreased in the steroid treated animals, whereas there were no alterations in the concentrations of plasma glucose, or serum total protein, magnesium, calcium, inorganic phosphorus, iron, copper, sodium and potassium.
Some modifications of behaviour were noted in steers implanted with the combined steroid preparation.



1596814136651.png

1596814175523.png
 

benaoao

Member
Which studies are you referring to when you state that studies agree that nandrolone creates more muscle than testosterone?

I am showing a study here that casts some serious doubt on that state. Comparison of the effects of high dose testosterone and 19-nortestosterone to a replacement dose of testosterone on strength and body composition in normal men - PubMed

Below is a breakdown of the study I posted on another thread.

View attachment 10137
those two for a start:



Re: your study. Consider how much water weight is being gained from all the extra E2 when injecting testosterone VS increased nitrogen on Deca (actual tissue) and you’re left comparing lean gains vs something you’ll leave in the toilet when backing down to TRT.
 

DS3

Active Member
those two for a start:



Re: your study. Consider how much water weight is being gained from all the extra E2 when injecting testosterone VS increased nitrogen on Deca (actual tissue) and you’re left comparing lean gains vs something you’ll leave in the toilet when backing down to TRT.
Vital pieces of information you are leaving out. The study I presented demonstrated both a substantial increase in body weight in the testosterone group versus the nandrolone group, as well as a significantly greater loss in body fat. That would conclude a greater increase in fat free mass in the participants in the T group over the N group.

Integral issue with the second study you present. The dosing frequency of Testosterone (blend of propionate, phenylpropionate, and decanoate) and Nandrolone was every two weeks. Of the dosage of T that was administered, 150 mg was either propionate or phenylpropionte and 100 mg was decanoate. What does that mean. That means that by the end of week one, the only T left in the participants system was the 100 mg of T decanoate. Due to the suboptimal administration of a blended testosterone preparation, the methods used are ill-equipped to compare the efficacy of 250 mg testosterone to 150 mg of nandrolone.

The first study you present does not offer the full article, but I would be skeptical that suboptimal methods were used similar to your second study.
 
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readalot

Member
I wrote up some comments on another forum in response to a question related to these anecdotal data:


This guy captured lots of blood work and couldn't understand or didn't want to offer a hypothesis as to why his systolic BP shot up. He tried to rule out effect of aldosterone.

The effect of nandrolone on β1- and β2-adrenergic receptors in the heart don't get near enough attention in my mind. I hope this may help someone who's weighing reward vs risk of anabolic therapy and especially the use of nandrolone for its anabolic effects. I know the risk/reward is different depending on the individual, but hope more folks will be aware of escalation in their pulse pressure or even drop in the their diastolic pressure and what the heart may be indicating.


Some additional examples (anecdotal of course) and discussion of HED from the animal studies (this is the original thread that started out as a question about topical nandrolone usage):

 
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readalot

Member
Alongside TRT; no intelligent person takes nandrolone alone.

It is unlikely that anyone on this forum will be able to provide a research example of why this reduction in TT occurs, aside from posting the relative binding affinities of Test and Nandrolone. Competitive binding at the androgen receptor is what I ‘believe’ to be the mechanism. I’ve seen this reduction in labs when I have taken nandrolone alongside TRT. Nandrolone has a much higher binding affinity for the androgen receptor than testosterone.

@Jason Sypolt had previously discussed the same effect on TT when he was taking oxandrolone. However, not much change occurred with his free T.
Thanks for your efforts to capture this information and make careful and diligent corrections along with way. I've made some comments on this phenomenon along with my anecdotal data here:



Correct me if I am wrong, but I haven't seen the relationship between SHBG and the metabolic clearance rate** of testosterone being brought up explicitly when analyzing this issue.

(EDIT: this is apparent metabolic clearance rate when basing production rate erroneously on Total T instead of free T or MCRx as per @Cataceous 's notation)

The effect of oxandrolone on SHBG much more pronounced than nandrolone, but in my experience both drop SHBG (nandrolone 20% and oxandrolone crushes it). So competing effects on total T (lower SHBG increases MCRx of Testosterone and lowers Total T measured by LC/MS for a given T dose measured at trough) vs free T (lower SHBG increases free T percentage of total). Where you end up on Total and Free T are a function of your SHBG response to adding in the additional AAS.

Here's the explicit blow by blow analysis since there's so much back and forth:
 
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DS3

Active Member
I wrote up some comments on another forum in response to a question related to these anecdotal data:


This guy captured lots of blood work and couldn't understand or didn't want to offer a hypothesis as to why his systolic BP shot up. He tried to rule out effect of aldosterone.

The effect of nandrolone on β1- and β2-adrenergic receptors in the heart don't get near enough attention in my mind. I hope this may help someone who's weighing reward vs risk of anabolic therapy and especially the use of nandrolone for its anabolic effects. I know the risk/reward is different depending on the individual, but hope more folks will be aware of escalation in their pulse pressure or even drop in the their diastolic pressure and what the heart may be indicating.


Some additional examples (anecdotal of course) and discussion of HED from the animal studies (this is the original thread that started out as a question about topical nandrolone usage):

I follow moreplatesmoredates' videos from time to time. I find the self-experiments he does interesting but never assign to much value to his results given the lack of reliability (repeatability within broader groups of people wherein the same results were maintained) generalizability (ability to generalize findings to large audiences) from case studies.

β1- and β2-adrenergic receptors in the heart is an interesting hypothesis for the rise in BP seen in males using nandrolone. I do not have much knowledge regarding what those receptors do or what role they could play in nandrolone-induced hypertension. However, Dr. Thomas O'Conner's (anabolic doc) explanation of aldosterone being the primary suspect does make sense to me given the concurrent rise in fluid retention seen in men taking nandrolone.

Regardless it nandrolone-induced hypertension is caused by changes in the heart's β1- and β2-adrenergic receptors or aldosterone, would it make a difference in the outcome? Would treating this induced hypertension be enhanced by knowing one way or the other? Or would limiting the dosage and length of administration still be the most effective way to combat long-term side effects such as left-ventricular hypertrophy?

 

DS3

Active Member
Thanks for your efforts to capture this information and make careful and diligent corrections along with way. I've made some comments on this phenomenon along with my anecdotal data here:



Correct me if I am wrong, but I haven't seen the relationship between SHBG and the metabolic clearance rate of testosterone being brought up explicitly when analyzing this issue. The effect of oxandrolone on SHBG much more pronounced than nandrolone, but in my experience both drop SHBG (nandrolone 20% and oxandrolone crushes it). So competing effects on total T (lower SHBG increases MCR of Testosterone and lowers Total T measured by LC/MS for a given T dose measured at trough) vs free T (lower SHBG increases free T percentage of total). Where you end up on Total and Free T are a function of your SHBG response to adding in the additional AAS.

Here's the explicit blow by blow analysis since there's so much back and forth:
You've brought up some very interesting points here!

@Cataceous is the only source I would really trust when discussing SHGB and its effects on TT, Free T, and metabolic clearance rate of testosterone. From previous evidence-based discussions with @Cataceous, I believe he has said that lowered SHBG does not increase metabolic clearance rates substantially. Hopefully, he will weigh in here. Also, it has been established on this forum, and primarily from the evidence that @Cataceous has presented, that in order to maintain consistent Free T levels, TT does lower in response to a decrease in SHBG.

Are you stating this just as an FYI or are you discussing the reduction in SHBG and TT in relation to a nandrolone-related side effect?
 

readalot

Member
You've brought up some very interesting points here!

@Cataceous is the only source I would really trust when discussing SHGB and its effects on TT, Free T, and metabolic clearance rate of testosterone. From previous evidence-based discussions with @Cataceous, I believe he has said that lowered SHBG does not increase metabolic clearance rates substantially. Hopefully, he will weigh in here. Also, it has been established on this forum, and primarily from the evidence that @Cataceous has presented, that in order to maintain consistent Free T levels, TT does lower in response to a decrease in SHBG.

Are you stating this just as an FYI or are you discussing the reduction in SHBG and TT in relation to a nandrolone-related side effect?
Purely for discussion and scientific debate/understanding. Was reading your detailed posts (and methodical nature) and thought I would add my 2 cents and my anecdotal data. Thanks!
 
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DS3

Active Member
Purely for discussion and scientific debate/understanding. Was reading your detailed posts (and methodical nature) and thought I would add my 2 cents and my anecdotal data. Thanks!
Love it! I appreciate the input.

So adding to our anecdotes here, what has your experience been with nandrolone? Do you experience any side effects from it or do you tolerate it fairly well?
 

readalot

Member
I follow moreplatesmoredates' videos from time to time. I find the self-experiments he does interesting but never assign to much value to his results given the lack of reliability (repeatability within broader groups of people wherein the same results were maintained) generalizability (ability to generalize findings to large audiences) from case studies.

β1- and β2-adrenergic receptors in the heart is an interesting hypothesis for the rise in BP seen in males using nandrolone. I do not have much knowledge regarding what those receptors do or what role they could play in nandrolone-induced hypertension. However, Dr. Thomas O'Conner's (anabolic doc) explanation of aldosterone being the primary suspect does make sense to me given the concurrent rise in fluid retention seen in men taking nandrolone.

Regardless it nandrolone-induced hypertension is caused by changes in the heart's β1- and β2-adrenergic receptors or aldosterone, would it make a difference in the outcome? Would treating this induced hypertension be enhanced by knowing one way or the other? Or would limiting the dosage and length of administration still be the most effective way to combat long-term side effects such as left-ventricular hypertrophy?

You bring up a good point...whether it's solely aldosterone or beta receptor mediated or a combination, in my particular case I am concerned with pro-arrthymic effects as well as any long term LVH concerns. In this context it may not make a difference to course of action as aldosterone shows similar effects:


Therefore, if one was really cautious they'd probably leave the nandrolone alone unless the reward somehow far outweighed the risk. That's the call for the clinician and patient to discuss but just wanted to bring up this angle as I don't think most ND users really appreciate the potential concern and ramifications. Especially if they are also taking liothyronine, work out very hard, middle aged, etc. It lines up as a potential synergistic land mine for athletes and the athlete's heart phenomenon.
 

readalot

Member
You've brought up some very interesting points here!

@Cataceous is the only source I would really trust when discussing SHGB and its effects on TT, Free T, and metabolic clearance rate of testosterone. From previous evidence-based discussions with @Cataceous, I believe he has said that lowered SHBG does not increase metabolic clearance rates substantially. Hopefully, he will weigh in here. Also, it has been established on this forum, and primarily from the evidence that @Cataceous has presented, that in order to maintain consistent Free T levels, TT does lower in response to a decrease in SHBG.

Are you stating this just as an FYI or are you discussing the reduction in SHBG and TT in relation to a nandrolone-related side effect?
I think these "greatest hits" are what you are referring to...


Particularly this exchange...starting here and scrolling down is gold:


My point was that you need to invoke the effect of the secondary AAS (you added to your protocol) on SHBG when you want to understand why your TT drops. Thanks for reminding me to look up @Cataceous 's posts on SHBG/free T/Total T. Very nice.

And for the record I'll amend my post above to substitute "MCR" for "apparent MCR when erroneously basing the production rate on Total T or MCRx" :)
 
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DS3

Active Member
I think these "greatest hits" are what you are referring to...


Particularly this exchange...starting here and scrolling down is gold:


My point was that you need to invoke the effect of the secondary AAS (you added to your protocol) on SHBG when you want to understand why your TT drops. Thanks for reminding me to look up @Cataceous 's posts on SHBG/free T/Total T. Very nice.

And for the record I'll amend my post above to substitute "MCR" for "apparent MCR when erroneously basing the production rate on Total T" :)
That's the post! @Cataceous' equation and explanation go over my head, but that was the conversation I was referring to.
 

readalot

Member
Love it! I appreciate the input.

So adding to our anecdotes here, what has your experience been with nandrolone? Do you experience any side effects from it or do you tolerate it fairly well?
I've provided a short, very short summary here. Unfortunately I can't pinpoint the experience to any one thing, but Testosterone+T3(combination Thyroid therapy actually)+ND use + HIIT + age probably were the perfect storm. Just want others to avoid the same experience as the road back is a long one from mental perspective.

Anabolic therapy for the proper indication can be helpful, but the side effects and tradeoffs when finding the optimum aren't exactly known beforehand.
 
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DS3

Active Member
I've provided a short, very short summary here. Unfortunately I can't pinpoint the experience to any one thing, but Testosterone+T3(combination Thyroid therapy actually)+ND use + HIIT + age probably were the perfect storm. Just want others to avoid the same experience as the road back is a long one from mental perspective.

Anabolic therapy for the proper indication can be helpful, but the side effects and tradeoffs when finding the optimum aren't exactly known beforehand.
Glad you are okay. Hopefully, the anxiety/panic attacks is improving?

It really is so fascinating how we have guys on here in their 30s, 40s, 50s, maybe even 60s, who take doctor prescribed nandrolone alongside TRT and feel great both physically and mentally. Then, there are cases like yours or mine that baffle those who respond favorably. You are right in the post that you linked; you never know how you will respond.
 

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