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Topical Nandrolone w/ TRT

Hey All,

Just saw this topic discussed on More Plates More Dates YouTube channel. Does anyone have experience with this and/or have any data around the efficacy of a topical application?

Thanks,
Alex

No data to help, but watching the topic with interest. Many years ago when I worked in a skin care laboratory, we did experiments to see if esterified vitamin A could affect the skin similarly to topical retinoic acid. Library research showed that all the necessary enzymes are present in the skin to break the ester bond and reduce the Vitamin A alcohol to the acid.

We used hairless mice in the experiment and indeed, we did show a dose-response to the amount of Vitamin A ester applied to the skin. The outcome measures were epidermal cell turnover and deposition of new collagen in the dermis as determined by histologist preparations. All standard tests at the time for the drug industry in assessing effectiveness of retinoic acid.

The results showed that indeed, esterified Vitamin A did have a similar effect as the retinoic acid controls and was dose dependent. Translating this to TRT and or topical nandrolone, we know that the enzymes necessary to cleave the ester are present in the skin. And we know from topical T preparations currently available that T does penetrate through the dermis. Does it have a similar effect and at what topical dose? That has (to my knowledge) yet to be determined.

Nandrolone is not a TRT drug.

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https://poddtoppen.se/podcast/1424766141/more-plates-more-dates/deca-only-for-hrt-a-comprehensive-overview-and-my-personal-blood-work
https://www.researchgate.net/publication/299434709_Beyond_testosterone_cypionate_Evidence_behind_the_use_of_nandrolone_in_male_health_and_wellness

Nice articles stating the known affects of Nandrolone… increased muscle mass and joint relief via increases in synovial fluid. All well known. Again… not a TRT drug. Not by the basic premise or the fact that it provides ANY long term health benefits. Quite the opposite. There is a reason no GP or Endo will prescribe it and is only available by clinics that make money to prescribe you drugs.

If you want to use Nandrolone, cool. But that belongs in the pharma section.

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The articles (one was edited out by the mod) and many other articles out there are basically studying nandrolone as an alternative for TRT. Why do you think all these other steroids were created in the first place. For various medical applications. It’s just the stigma against them has overshadowed that. So to you they are strictly PED’s…great.

Not to me… to all those seeking their use as an adjunct to replacement therapy. Quite simply we have testosterone for TESTOSTERONE REPLACEMENT THERAPY. The only benefits to using Nandrolone are those I listed above. Nandrolone was developed as you said ‘for various medical applications’. The wasting diseases it is legit prescribed for are generally more detrimental to your health than the side effects of Nandrolone use. Also, anecdotally, you will see TRT clinics prescribing it in higher doses than those that do legitimately use it for wasting diseases.

Well it’s also referred to as HORMONE REPLACEMENT THERAPY but heaven forbid since this is “T” Nation and the “T” Replacement forum (rolls eyes)

So you are proposing you are replacing your “lost or deficient” Nandrolone now? I’ll ignore the eye roll and keep it academic. Clearly we will agree to disagree but at least others get to see different view points.

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And to bulk cattle up before slaughter, or make horses run fast. Some of the newer AAS were designed just for lifting weights and building muscle. Stuff like superdrol and epistane IIRC.

Nandrolone is naturally present in the body IIRC. However, it is present in such small amounts that replacement for it would yield essentially no benefits.

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I post too much detailed scientific boring stuff on here. So I am going to go out on a limb with some entertainment. Here’s my impression of nandrolone only HRT. Yes, I get some leeway here so this is effectively time lapsed:

I’ve got 10 mL of 200 mg/mL ND that will continue to just sit there as a curio.

I posit ND-based HRT is a good example of Dunning-Kruger effect with respect to risk vs reward.

Not picking on anybody, as I myself have been guilty of using in a TRT protocol.

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How did this post get so badly hijacked? The guy asked a simple question and somehow this has gotten into a debate over what is and is not TRT or HRT? Give it a rest and get back on topic!

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Sorry readalot. Did mean for that to be a reply to you. It was supposed to be a general reply to the thread.

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@youthful55guy no worries and good point. I really enjoy your graphs, nice work!

Back to the topic, if you wanted to do nandrolone topically, you wouldn’t use the ester (although your comments are well taken and using the ester would be potentially feasible but with very low absorption).

@irocktheyellow, you’d use nandrolone USP since there is a reference standard and you could compound that just like testosterone with the USP bulk.

But again you wouldn’t want to (hence my poor attempt at humor with the video above). So what’s driving my bias? The guy you linked (see the More Plates More Dates web article dated Feb 1, 2020) to does a meticulous job with the blood work but never connects the dots on the isolated rise in systolic blood pressure. It’s a subtle tell that I don’t see ever getting discussed properly.

What’s my hypothesis for this?

What he doesn’t mention is that nandrolone can strongly upregulate beta-1 / beta-2 adrenergic receptors in the heart (dose response much more potent that testosterone):

Significance

This study indicated that nandrolone, whether associated with resistance training or not, induces cardiac hypertrophy, which is associated with enhanced collagen content, re-expression of fetal genes the in left ventricle, and impaired diastolic and systolic function.

Abstract

To investigate whether nandrolone decanoate (ND)-pretreatment can modulate (1) beta-adrenoceptor expression and (2) myocardial contractility in response to beta-adrenoceptors stimulation with isoproterenol (ISO), in hearts of both normal and stressed rats. Rats were treated with 15 mg/(kgday) of Deca-Durabolin (ND, 1 ml i.m.) or with vehicle (oil) for 14 days. The day after the last injection, the dose-response to ISO (1 x 10(-8), 5 x 10(-8) and 10(-7)M), was studied in isolated rat hearts harvested from unstressed animals (unstressed+vehicle (control) or unstressed+ND) or from stressed animals (stressed+vehicle or stressed+ND): acute stress protocol consisted in restrain for 1h immediately before sacrifice. ND-pretreatment increased beta(2)-adrenoceptor expression. In baseline conditions all hearts had a similar left ventricular developed pressure (LVDP) and maximum rate of increase of LVDP (dP/dt(max)). In hearts of unstressed+vehicle or unstressed+ND, ISO caused a similar increase in LVDP (+90-100%) and dP/dt(max) (+120-150%). However, hearts of stressed+vehicle animals showed a marked depression of inotropic response to ISO (i.e. for ISO 1 x 10(-8),-55% in LVDP response versus unstressed). Yet, in hearts of stressed+ND-animals the effect of stress was reversed, showing the highest response to ISO (i.e. for ISO 1 x 10(-7), +30% LVDP response versus unstressed). The ND-induced beta(2)-adrenoceptor overexpression does not affect ISO-response in unstressed animals. However, acute stress induces a down-regulation of ISO-response, which is reversed by ND-pretreatment. Since the physiological post-stress down-regulation of adrenergic-response is absent after nandrolone treatment, the heart may be exposed to a sympathetic over-stimulation. This might represent a risk for cardiovascular incidents in anabolic steroid addicts under stressing conditions.

Abstract

Aims

This study was performed to assess isolated and combined effects of nandrolone and resistance training on the blood pressure, cardiac electrophysiology, and expression of the β1- and β2-adrenergic receptors in the heart of rats.

Main methods

Wistar rats were randomly divided into four groups and submitted to a 6-week treatment with nandrolone and/or resistance training. Cardiac hypertrophy was accessed by the ratio of heart weight to the final body weight. Blood pressure was determined by a computerized tail-cuff system. Electrocardiography analyses were performed. Western blotting was used to access the protein levels of the β1- and β2-adrenergic receptors in the right atrium and left ventricle.

Key findings

Both resistance training and nandrolone induced cardiac hypertrophy. Nandrolone increased systolic blood pressure depending on the treatment time. Resistance training decreased systolic, diastolic and mean arterial blood pressure, as well as induced resting bradycardia. Nandrolone prolonged the QTc interval for both trained and non-trained groups when they were compared to their respective vehicle-treated one. Nandrolone increased the expression of β1- and β2-adrenergic receptors in the right atrium for both trained and non-trained groups when they were compared to their respective vehicle-treated one.

Electrocardiographic Profile and Muscle Glycogen Content of Rats Treated with Nandrolone

I can post these all day. When I used ND along with TRT I watched my pulse pressure (systolic minus diastolic) slowly increase from 40 mmHg to over 60 mmHg. The systolic kept going up and diastolic dropped 10 points.

Take a look at this:

Circulating Catecholamines

Guess what the ND effect on BP looks just like: that’s right, acute dosing of epinephrine.

So your sensitizing your heart to catecholamines you naturally produce and potentially changing the morphology and electrical signalling of your heart. This is not stuff you want to mess with long term, especially as part of some replacement strategy.

I fell for all this too originally even after meticulous research (but not meticulous enough). In my case I was also doing combination thyroid treatment, and I am sure there was interplay there between the lithyronine and ND. Went a little to high on testosterone and voila, went into AFIB.

Please leave the nandrolone (nortestosterone derivatives) alone if you value your long term health.

BTW, You may get collagen synthesis, just not where you want it (heart instead of joints). Also, please someone point me to one reputable source that shows nandrolone has any localized effect on synovial fluid. Given what we know about chronic pain and perception, my hypothesis is the significant effect of ND on chronic pain/join pain happens at the brain (neurotransmitters), not regeneration of the joint.

There we go, back on topic. Thanks @youthful55guy.

Seriously, if you guys take the time to read anything on here, study up on this. ED, mood swings are serious concern, but not as serious as long term electrical issues with the heart and CARDIOVASCULAR complications from nandrolone.

EDIT: Also, proper recognition to @unreal24278 who has daylighted these concerns in previous threads (after just searching the archives).

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Now that is interesting and something that I did not know. Thanks for sharing!

It appears that 2 of the 4 studies showed equivalent usage rates of 8mg/kg/wk, 1 mentioned 15 mg/(kgday) (I don’t know how to convert that) and one study did not specify dosage… That seems like a metric shit ton of gear. for me that would be 900 mg/wk, I’m using a little more than 1/3 of that. I understand there is inherent risk associated with all AAS usage, but these studies don’t seem to be in line with casual AAS users, and ALMOST seem like a scare tactic (not from you but from the individuals running the study).

What am I missing here? There are people much smarter than I on this forum, but this is how I interpret those studies. Can someone clarify this for me?

Dude, this is a terrific idea… But let’s turn it up a notch and add in some beta-2 agonists. Beta adrenergic receptors desensitise fairly quickly, add in something that can slightly offset this.

Perhaps, we don’t have enough literature to go on relating to potential pain-blunting mechanisms. Furthermore, the majority of the data we have at had pertains to rodent models. Rats have different metabolic/elimination pathways/enzymes and as a result results garnered within rodent models can differ when the same stimulus/exposure is give to a human.

I can link some data relating to the impact of nandrolone on healing rates regarding tendon rupture/injury. I don’t spend all that much time on the Pharma section nowadays. Talking about anabolic steroids online just seems like a bad idea.

Not really, the concept of HED is important. A human equivalent dose for 8mg/kg for a 100kg male would be around 130mg/wk. Interestingly testosterone dosages of around 5mg/kg induce cardiac pathology within rodent models.

There’s an in-vitro study of which indicates nandrolone is likely more destructive when regarding vascular health. The study design is rather poor, but it grants further evidence to state nandrolone should probably be left out if longevity is at hand. The researchers expose endothelial cells (in vitro) to nandrolone, nandrolone metabolites, testosterone etc. Androgen concentrations were increased until 50% of the cells present had undergone apoptosis. Nandrolone did so at a concentration 11x lower than testosterone (the concentration was still massive as the effect had to be garnered within an acute timeframe)

15*100 (lets say you’re 100kg) * 7
/6.2 = 1693.5

My left ventricle would explode…

All AAS seem to have an effect regarding catecholamine up-regulation. Some are more sensitive to the autonomic destabilisation induced via AAS, hence arrhythmias, resting tachycardia/increased pulse rate etc. Nandrolone/19-nors and testosterone appear to be particularly potent, haven’t seen much data on other synthetics.

I was a little unclear, according to the one study, it was called out that the dosages used on rats (5mg/kg 2x/wk) were equivalent to a human using 8mg/kg/wk, which for a 100kg person would be 800 mg/wk, or for me that would be 896 mg/wk.

image

Careful, it is not that simple:
image

You need a conversion factor of ~6 to convert to HED:

https://www.fda.gov/media/72309/download

So three of the studies I posted have animal dose of 10 mg/kg/week (close to the 8 mg/kg/week mentioned in the other study but they are comparing an animal dose to anecdotal human dosing) but that’s really only 1.6 mg/kg/week for human based on body surface area ratio.

Here’s the summary for the above papers I cited:

image

As @unreal24278 just mentioned, reference 3 HED is high but look at refs 1, 2, and 4. You already have the anecdotal data from moreplatesmoredates and me. Doesn’t take much ND to move BP as I described. Does that help?

Thanks for highlighting. The authors are incorrectly comparing the rat dosing (10 mg/kg/wk) to the anecdotal human dosing (8 mg/kg/week). Correcting for the ratio of body surface area per unit mass, the HED for the rat study is 1.6 mg/kg/week.