Usually I’d just leave this info “buried” in the other thread but it’s important enough to daylight it on the main page. Nandrolone based “HRT” and nandrolone use for joint/pain relief continues to garner much discussion and attention and it’s picking up.
Please care for yourself. Your long term cardiovascular health is much more important than some short term muscular gain.
Please see below. This was pasted from post on the TRT forum:
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):
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.
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.
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.
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.
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.
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:
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 too 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).