T Nation

Read This Before Considering Nandrolone or Any AAS

Thank you sir for taking the time. It’s like pushing a rope sometimes. Obviously daylighted in the literature for those that dig, but I haven’t seen proper discussion of upregulated beta adrenoceptor expression in the heart wrt nandrolone use even in what may seem to be low, “therapeutic” dosing. It’s a complex subject and nandrolone use accompanied with widening pulse pressure appears subtle unless you know what you are looking at. I just want guys to consider the risks vs reward if they consider using nandrolone as part of anabolic therapy. It’s not all roses.

Mood swings and ED almost minor compared to inducing cardiac electrical dysfunction or potential HF.

I have thought about trying a low dose deca cycle eg 100mg/wk for 12 weeks plus test TRT dose(125mg) to see If I get joint relief. Then off for deca for 3 months, as opposed to taking deca all the time. Surely that would be a safer option than always being on low dose deca.
If find a little legit pharma seems to go a lot further than UGL gear. eg 250 of test seems to give me as much hypertrophy as 500mg of UGL test.
When I used to do genuine cycles with EQ, I got a lot of joint relief, that continued nearly all the way until the next cycle 3-4 months later.

I’ve glossed over this numerous times as a byproduct of talking about mechanisms behind AAS induced cardiotoxicity. The upregulation of beta adrenergic receptors/catecholamine sensitisation isn’t sole to Nandrolone either. Nandrolone/19-nors merely seem more potent with regards to inducing this unwanted side effect.

Hypothetically speaking, during vigorous exercise these aforementioned mechanisms could be enough to trigger arrhythmia. Throw in some pathologic LVH and it’s ventricular… Fibrillation… city…

That didn’t sound so smooth.

This is what I’ve read
“Despite some beneficial effects of anabolic androgenic steroids (AAS) compounds in improvement of physical performance, chronic using of high doses of these drugs is associated with numerous adverse effects on the cardiovascular system including hypertension, myocardial infarction, dysrhythmias, hypertrophic cardiomyopathy, and cardiac remodeling”
The research has been done on animals and mentions “chronic use of high doses” so I’m not sure if you can necessarily infer that low doses on humans for the purpose of taking advantage of some of the benefits would necessarily lead to the same negative issues. I can see that the research might give someone pause but I wouldn’t necessarily freak out about it either, especially if administered under doctors care/monitoring.

1 Like

Most people who use gear don’t run just a few cycles and/or dosages below 3-500mg/wk. It’s typically upwards of 1 gram +, with 2-3 cycles per year for decades.

There will be a spectrum of individualistic predisposition towards negative side effects, but my outlined pattern of use will cause issues for most people 20-30 years down the line.

For whatever reason we tend to think about the here/now, because we can’t see damage being done we like to pretend it doesn’t exist. People should be more focused on long term rammifications/legitimate potential side effects. Erectile dysfunction, while shitty… Won’t kill you. Heart failure and/or cardiomyopathy might though.

Absoluely, that’s why I give you recognition over on the thread I linked to here. It’s understandable most of us will always be a few steps behind you :-). Thanks for all your efforts.

To give folks a flavor, see here:

Question, post a-fib episode you’ve specified you have symptoms pertaining to arrhythmia and/or autonomic dysfunction but can’t take beta-blockers due to associated side effects.

Have you spoken to an MD about using a medication such as ivabradine? If you’ve got a fast RHR this medication can be tremendously beneficial in regards to symptom management.

Have you tried cardioselective beta-blockers

It’s used off label for IST, isn’t associated with the same unwanted side effects (altered glucose tolerance, fatigue, dyspnea predominantly associated with no selective bb’s etc)

No one should have to suffer needlessly with autonomic dysfunction @readalot

Off topic, but I think propranolol in low doses can work wonders for social anxiety when taken on an “as needed basis”.

Thanks for taking the time. I gave three examples in the thread linked here, mine, moreplates more dates, and also @wsmwannabe gave his experience. I am sure there are many more out there. What prompted all this was the more plates report (link got nuked by the Mod but you can find it). Incredible amount of bloodwork but the guy didn’t understand why his systolic pressure shot up or didn’t want to hypothesize. I haven’t seen any discussion of widened pulse pressure using ND (or nandrolone in general) and what this could mean.

No discussion here:

Cardiovascular issues mentioned here in the context of illicit AAS use:

You guys correct me if it’s on Youtube. I haven’t seen any mention. So I think the idea I am communicating is that significant complications can happen at therapeutic dosing 100-150 mg/week, especially in synergy with T3 usage, underlying pathology or arrythmia, etc. I have only used therapeutic dosing less than 150 mg/week of ND with Rx. Moreplatesmoredates mentions 100 mg/week. @wsmwannabe is at a little over 3 mg/kg/wk. Don’t think this only can happen after years and some obscene dosages.

I hope guys watch their systolic numbers but also watch for drops in the diastolic pressure. Tracking BP and HR (as @mnben87 has thrown out is great), but explicitly watching your pulse pressure will also help. If your diastolic is dropping below 60 mmHg or pulse pressure increasing above 60 mmHg, that could be telling you something important.

I don’t want guys having to experience waking up 4 nights out of 7 at 2AM with heart racing because their heart has been sensitized to modest release of catecholamine during a dream. It is no fun and once your mind is involved (anxiety, panic, etc) it is a viscous cycle. If I can help a few people, then it was worth it. Unless you have an issue where reward far outweighs risk, please leave this stuff alone. I thought Anabolic Therapy for autoimmune/joint/rheumatoid issues was worth it. This book lays out all the pros:

https://www.google.com/books/edition/Anabolic_Therapy_in_Modern_Medicine/RPUqffuFXqIC?hl=en&gbpv=1&printsec=frontcover

But there is a dark side that I think is vastly overlooked (except for the powerful mind of @unreal24278) even for “therapeutic” dosing. I hope my thoughtful regurgitation of most of @unreal24278 's points with the pulse pressure observation helps you all make the right decision.

Interesting info about myself. I’ve always had low BP. My diastolic is frequently below 60, I’ve had it as low as 48! Resting BP is typically around 100/55.

Hey thanks for asking. I taking the less is more approach and back to levothyroxine monotherapy (took out the T3) combined with taking TRT back to 50 mg/wk of TC (yes the ester). Peak/trough is 900/300 ng/dL (once weekly sub-Q).

I have used metoprolol tartrate (fast acting) intermittently when I get really panicked. Gradually coming along with lots of cardio and getting my confidence back when pushing back up above 80% effort. I think this will be reversible.

300ng/dl is seriously on the low side. Wouldn’t you prefer to space out shots 2x/week and not have such a nasty nadir. Like 25mg 2x/wk sub q?

My nadir is like 550-600ng/dl

Notice the pulse pressure in your example is 45. Should mention that someone would track vs their baseline. But at your age if you BP was 100/55 (baseline) then went to 120/55 or 120/50 with nandrolone, that’s probably worth bringing up with your physician I think. Scary part is I have asked both cardiologist and well respected TRT doc about this and got hand waved.

Hey compared to the 80 ng/dL I experienced a few months ago when I went cold turkey, I am all good right now. That gave me a whole new appreciation for low T!

I’ve had widened pulse pressure on just about everything. Don’t recall if it was particuarly exacerbated when I tried Nandrolone. Nandrolone was definately the nastiest in terms of exacerbating autonomic dysfunction. Testosterone second… Dbol was probably the mildest within that regard, though my exposure to it was very minimal (short duration + conservatively dosed)

Why did you drop T cold turkey? Was this decision anxiety related or in response to instructions from a doctor?

Dropped the T3 and TRT partly because of cardiologist recommendation. TRT cold turkey no fun but was tired of the arrythmmia and Hct was still up at low 50s. Wanted to methodically add back in the lower dose TRT and see what happened. Hence, wanted to get my Hct back down to 45%, take out the T3 and start over. Hard to be completely stone cold scientific when you are feeling palpitations 24 hours a day. Thanks for asking.

Thank you for this. I have been on NPP, trying various doses, for months now. I have not experienced any positive effects and HAVE experienced many negative effects. I’ve been seriously considering stopping it recently and this tipped the scales for me. Thank you!

1 Like

Thanks so much for sharing your experience. My pleasure, and one by one, we can make a difference. Take care of yourself. Sometimes I feel like it’s shoveling dirt out of one hole and putting in another with all the posts on here asking to rationalize the proposed “cycles/regimens” aka drug abuse. It’s this type of feedback and dialogue that makes the posting worthwhile.

1 Like

Whilst I generally agree with what you’ve said, I think the level of risk one is willing to take varies from person to person. Some people may very well be comfortable with taking the risks associated with AAS use, and at that point, on an individualistic basis I don’t think it’s our place to judge.

If a healthy, mentally in-tact individual decides to use after being educated/well aware of the potential ramifications, then live and let live. Drug use, for better or worse is present within our society and won’t go away anytime soon. Anabolic steroids are no exception to this rule.

Many people come up with insane theories to justify unhealthy and/or destructive behaviour… I don’t understand why people can’t just be honest about this… don’t live in denial… (i.e “I know this is unhealthy, I know what I’m doing dramatically increases my risk for X,Y and Z and I’m okay with that, it’s my decision to make”).

I think if we can allow people to gouge themselves until they die prematurely, smoke, drink to excess, gamble and more we can tolerate an individualistic decision to use gear. I don’t really feel it’s my place to judge unless the person is

  • unaware of ramifications and stake and/or literally knows nothing about what they’re using
  • in denial about potential consequences
  • supplying/selling dangerous substances to other people

I don’t think everyone choosing to run cycles fits under the bill of being ignorant, unaware or in denial. I think a portion of adults using are well aware of the risks associated, but after making a benefit/risk analysis decided to use anyway. What constitutes as being beneficial, rewarding or important will dramatically differ from person to person.

2 Likes

Great summary! I was referring to the posts where someone puts up a list and then asks “Does this look good?” Or “hey, does this look like a low risk, leans gains stack?” Then someone will go the trouble of asking “Good for what?” Then no response. But you are absolutely right and wise beyond your years.

If 1 out of 100 gets self-awareness out of reading the valuable public service announcements you go to the trouble to post, then that is adding value. Thank you for your time man.

Nice introductory material for the interested reader.

Discussion

AAS has a protective effect on the cardiovascular system in the physiological dose range. However, supraphysiological AAS doses produce toxicity in the cardiovascular system, which significantly increases the cardiovascular risk [Figure 1]

The mechanism of AAS toxicity has not been fully elucidated. Studies demonstrated that there were two main mechanisms [Figure 2], one of which is AAS gene regulation where AASs or their metabolites bind to ARs, which leads to a conformational change of these receptors. AR dimers are then transported from the cytoplasm into the nucleus where the dimers bind to androgen reactive elements in DNA, thereby regulating gene transcription in cooperation with activation (or inactivation) of co-regulations, which results in toxic effects.[82] Another non-gene regulatory mechanism (mainly in skeletal muscle cells and prostate cancer cells) is that AR dimers bind to cytoplasmic proteins through a variety of signaling pathways that directly induce toxicity without gene transcription pathways.[82,83] The degree of AAS toxicity is related to a variety of factors such as dose, cycle, and individual differences. Through medical examinations, people taking AASs for a period of time or even a few years may not show any abnormal index results.