Left Ventricle Hypertrophy and Nandrolone ( Decadurabolin )

Dear Nelson Vergel and forum members,

I am a long time reader, first time poster, In fact I registered just to post these questions. While I have addressed this to Nelson specifically I would be very grateful for any evidence-based input from the members of this forum.

Let me first thank you, Nelson, for this website and all of the other science-based information you have put out. I have found your books, videos and sites extremely helpful!

I recently read your book, "Built To Survive" in which there is a section about nandrolone use. I also recently read the threads on this website about nandrolone as a part of TRT.

From my understanding of those threads Nelson, you used Nandrolone (decanoate?) for a decade at 200mg/week in combination with exogenous testosterone. However, you have stopped using nandrolone and one of the main reasons for that stoppage is that you have left ventricle hypertrophy and came across scientific literature which indicated nandrolone may lead to left ventricle hypertrophy. Is this correct?

This prompted me to do a thorough reading of the scientific literature on the subject of AAS and left ventricle hypertrophy. I wish to outline my understanding of the literature and seek your opinion and any other papers that I may have missed or misunderstood in my search.

My original posts contained links to several papers. Unfortunately the forum rules prohibited me fro posting links on my first post. So I have had to remove all the links to be able to post this. I have emailed the original post including the links to the papers to Nelson Vergel. If you are a member that would like to read these studies or Nelson, if you received my email and would like to post the links. I would be happy to oblige!

I understand that LVH is correlated with some forms of heart disease. However, it is my understanding that there is both pathological and non-pathological left ventricle hypertrophy. And that those who partake in regular, intense exercise tend to have some degree of left ventricle hypertrophy. This is called the, "athlete's heart." This form of left ventricle hypertrophy is an adaptation to the extra demands placed on the heart during rigorous exercise and as long as the thickness of the left ventricle does not exceed a certain limit and cardiac function is not effected, then this hypertrophy is not considered indicative of a heart issue. I assume that, at least in part, your LVH is due to exercise adaptations. Do you mind me asking if you also have cardiac dysfunction and if so did the onset correlate with the use of nandrolone? If so, has this dysfunction resolved since cessation of nandrolone use? Has your LVH regressed since cessation of nandrolone use?

I am aware of several in vitro and animal studies which seem to show that nandrolone specifically, (and perhaps AAS, excluding testosterone in general?) may increase LVH and cardiac dysfunction.

nandrolone molecule vs testosterone.webp


The contentions I have with these studies are, of course, that they are not human studies. They are often poorly designed and controlled. Animal studies tend to use supraphysiological doses (5-15mg/kg/ day-week) for long periods of time (while many of these studies last only 8-16 weeks, this is actually quite long for a mouse with a lifespan of 2-3 years). Also, these animal studies do not combine testosterone with nandrolone. It is my understanding that low t levels predispose humans (and presumably other animals) to heart disease and testosterone replacement lowers this risk. It is also my understanding that nandrolone will cause a decrease in endogenous serum t levels, so isn't it possible that co-administration of exogenous t with nandrolone could prevent or offset some of the purported deleterious effects of nandrolone on the heart? Furthermore, the studies that show deleterious effects fail to study the animals after cessation of nandrolone use. Are the effects permanent or reversible? I could only find one rat study on this matter which seems to indicate the effects are reversible


And this animal study actually found pretreatment of mice with 15mg/kg/day for 2 weeks did not alter cardiac weight, increased expression of beta2-adrenoreceptors in the heart and reduced post-ischemic cardiac infarct size.


Nandrolone is associated with increases in ferritin, hematocrit, hemoglobin, blood pressure, and effects cholesterol. These are all predisposing factors for heart disease. Educated humans understand this and can manage (most of) these factors. The animal studies do not phlebotomize the animals or manage these issues. Perhaps much of the ill-effects of nandrolone on the animal heart could be resolved by managing these issues?


I am very wary of the case studies of athletes who had a heart health issue; upon interview or autopsy, AAS use was discovered and then the authors speculated about AAS being the cause of their heart issues. In my opinion, these studies are dubious for several reasons, which I assume will be apparent to you. Correlation does not equal causation. These subjects should have LVH based on their exercise regimen alone, a fact that rarely seems to be considered by the researchers when examining the subjects' hearts. Considering the millions of AAS users worldwide, the few case study subjects with heart problems appear to be an exception rather than the norm of AAS use. Furthermore, other factors are not controlled for such as their diet, sleep, alcohol, cigarette, drug use, family history of cardiovascular disease, etc, etc, etc., These users, for the most part were using supraphysiological doses of several drugs for extended periods of time.

Even still, many of these case studies do not support the notion that AAS exhibits cardiac toxicity.


In my opinion the most well designed studies (and most pertinent for us) are human studies on nandrolone that have either identified AAS users and monitored them before, during and or after AAS use or (creme de la creme) are blinded, randomized, placebo controlled trials.

Below is a list of all the human studies I could find:

1)

This is a double-blinded, randomized, placebo controlled human study of 200 mg/wk x 4 wk of nandrolone in which the authors concluded that nandrolone had no effect on cardiac function compared to placebo.

2)

This paper has 2 studies. The first is 12-16 week AAS use compared to non-use, The second is a double-blinded, placebo controlled trial in which subjects received 200 mg/wk i.m. nandrolone x 8 wk.
The authors concluded that there were no changes in heart structure or function.

3)

This study compared the hearts of AAS using and non-using weightlifters to endurance athletes. The authors concluded, "There is no evidence that LV ejection fraction in elite athletes is altered by either type of training or AAS misuse."


4)

This study found no difference between the structure and function of the hearts of AAS using and non-using weightlifters. These AAS users used multiple drugs for multiple cycles.

5)

This study found no difference in the hearts of AAS using and non-using body-builders.


6)

This study found that myocardial changes due to AAS use did not shorten ejection fraction and any structural changes reversed after 8 weeks off AAS.

7)

This study of AAS using and non-using bodybuilders found an increase in LVH but no dysfunction.

8)

This study indicates that Growth hormone+ AAS may be more responsible for structural and functional changes in the heart than AAS alone and that the impact of AAS on the heart may be reversible.


9)

This study followed 20 previously non-using AAS bodybuilders for two years as they began their AAS use and assessed long-term effects. Many of the bodybuilders AAS use included nandrolone. The researchers found no changes in the heart's structure or function during the two years of AAS use.


While some animal studies indicate there could be some adverse cardiac effects with long-term, supraphysiological nadrolone use the human studies, in my opinion, do not support this notion.

Nelson, I understand that you were using nandrolone for 10 years and I could not find any studies on animals or humans about the effect of such long-term use, so extra caution should be taken. But, if one were interested in cycling in 100 mg nandrolone for 6-8 weeks every two years of a life-long 150 mg testosterone weekly TRT regimen, say for joint and tendon issues as well as anemia, and if one were managing their hematocrit and hemoglobin with blood donation, if blood pressure and cholesterol were monitored and kept normal, do you see any cause for concern that nandrolone might permanently damage the heart? Do you know of any other potentially fatal adverse effects that might be associated with this kind of nandrolone use? Do you have any other human studies that support your position?

Finally, do you believe the use of low intensity endurance exercise,diet,or supplementation with coq10 or d-ribose could be of benefit in preventing any potential unwanted cardiac effects, if one were to cycle nandrolone in the above stated manner?

Nelson, what are your thoughts on decanoate vs phenylpropionate for 6-8 weeks of 100 mg/wk with test at 150 mg?

Thank you for your time. I eagerly await your response(s).
 
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Hi Mopes,

Your experience is very encouraging.

It sounds like you are making the right decision to get blood work done before deciding if ancillaries are necessary.

I was once convinced I was getting gyno and when my blood work came back everything was in the normal range and all my "symptoms" just disappeared. Totally, psychosomatic in my case.

I am very interested to see your blood work. Please keep me posted.

I think you may be interest in taking a look at some of the research on stanozolol in regards to collagen, joint, and bone health:

1) This is a nice double blind, human study showing that 10mg stanozol/daily for 6 months showed a significant improvement in arthritic symptoms compared to placebo. The authors speculate that it is stanozolol's fibrinolytic enhancing activity that mediated the response.

https://academic.oup.com/qjmed/arti...Effect-of-Increasing-Fibrinolysis-in-Patients

2) This paper found that 10mg/daily of stanozolol decreased symptoms of arthritis AND increased blood and joint fibrinolysis.

http://ard.bmj.com/content/annrheumdis/43/6/774.full.pdf

3) This study showed that in patients with osteoporosis 5mg/daily stanozolol for 1 year increased bone formation rate twofold and increased wall thickness at endocortical sites.

http://europepmc.org/abstract/med/1657503

4) This study of postmenopausal women with osteoporosis found that 29 month sof stanozolol increase total body calcium and regional bone mass. I can't access the full paper so I don't know that dose. Adverse effects were not severe enough to terminate treatment.

5) This study on sheep found that injections of stanozolol into the knee after a surgucal menisectomy was performaed resulted in significant regeneration of articular cartilage.

http://www.sciencedirect.com/science/article/pii/S0034528812003797

6) Here are three studies showing intraarticular stanozolol injections decreased lameness in horses

http://www.sciencedirect.com/science/article/pii/S0737080615005110

http://www.sciencedirect.com/science/article/pii/S073708061400464X

http://www.sciencedirect.com/science/article/pii/S0737080616300946

7) Here are a few in vitro studies showing stanozolol stimulates collagen synthesis

https://link.springer.com/article/10.1007/BF01967415?LI=true

http://s3.amazonaws.com/academia.ed...=Stimulation_of_Collagen_Synthesis_by_the.pdf

https://www.infona.pl/resource/bwmeta1.element.elsevier-3030a0d3-b99b-3a01-8c35-3effdd77af3f



I find it interesting that in the bodybuilding community stanozolol is notorious for inducing joint pain when these studies indicate that it would actually help joints. I guess it may have to do with the much larger doses bodybuilders are using compared to these studies. The wikipedia page author claims:

"Stanozolol as a DHT derivative can selectively compete with progesterone and other natural and synthetic progestins (nandrolone) for progestin receptors; yielding a reduction in progesterone mediated anti-inflammatory processes and presenting patients with a perception of increased joint discomfort."

There is no citation given though.
 
Got bloodwork back after six weeks on weekly dose of 210 T cyp and 210 nandrolone. Injections were on an EOD basis. Feeling good but nandrolone does not seem to do my lipids any favors. Never seen my lipid panel this bad even on similar or higher T doses.

Been taking 500mg citrus bergamot w coq10 twice a day for some lipid support. Have now added in plant sterols and aged garlic to see if I can stabilize things a bit. If not will have to discontinue.

Prolactin is higher than I've seen before, much like I assumed. Pre nandrolone prolactin was 8.8 ng/mL.

Estradiol is in line with what I would expect and doesn't seem to be impacted by nandrolone at all, which given it's rate of aromatization, or lack thereof, makes sense.
 

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HDL decreases on nandrolone and higher dose TRT. Everything else looks OK. It seems that you are not working out that hard.

Nelson, you are certainly correct. Workout intensity has dropped dramatically the past 9 weeks as a result of torn MCL which I am rehabbing.

Very curious what would allow you to draw that conclusion (that I'm not working out that hard) strictly from the blood work?
 
Rat study: Rapamycin improved hypertrophy & ejection fraction in rats with early heart failure

Effects of rapamycin on autophagy of myocardial cells in rats with early heart failure

Results: At 4 weeks after rapamycin intervention, significantly higher left ventricular ejection fraction (LVEF) was observed in the treatment group compared to the control group (P<0.05); but there were substantial reductions in the left ventricular posterior wall thickness at end-systole (LVPWs), the inter-ventricular septum thickness at end-systole (IVSTs), the left ventricular posterior wall thickness atend-diastole (LVPWd) and in the inter-ventricular septal thickness at end-diastole (IVSd) (P<0.05). The autophagy rate of myocardial cells was significantly lower in the treatment group versus the control group (P<0.05).

Compared to the sham group, the levels of proteinsBeclin-1 and Cathepsin D expression significantly improved in the control group (P<0.05), but reduced markedly in the treatment group (P<0.05).

Conclusion: Reductions in the autophagy of myocardial cells and improvements in the cardiac functions of rats with heart failure by rapamycin may be attributable to regulation of the expression levels of proteins Beclin-1 and Cathepsin D.
 
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Pharmacological Inhibition of mTOR Kinase Reverses Right Ventricle Remodeling and Improves Right Ventricle Structure and Function in Rats.
Pulmonary arterial hypertension (PAH) is characterized by pulmonary vascular remodeling, increased pulmonary artery pressure (PAP), right heart afterload and death. Mechanistic target of rapamycin (mTOR) promotes smooth muscle cell proliferation, survival and pulmonary vascular remodeling via two functionally distinct complexes, mTORC1 (supports cell growth) and mTORC2 (promotes cell survival), and dual mTORC1/mTORC2 inhibition selectively induces PAH PAVSMC apoptosis and reverses pulmonary vascular remodeling. The consequences of mTOR inhibition on RV morphology and function are not known.

Using SU5416/hypoxia rat model of PH, we report that, in contrast to activation of both, mTORC1 and mTORC2 pathways in small remodeled PAs, RV tissues had predominant up-regulation of mTORC1 signaling accompanied by cardiomyocyte and RV hypertrophy, increased RV wall thickness (RV WT), RV/LV end-diastolic area (EDA) ratio, RV contractility (max dP/dT) and afterload (Ea), and shorter RV acceleration time (RV-AT) compared to controls. Treatment with mTOR kinase inhibitor PP242 at weeks 6-8 post-PH induction suppressed both mTORC1 and mTORC2 in small PAs, but only mTORC1 signaling in RV, preserving basal mTORC2-Akt levels. Vehicle-treated rats showed further PH and RV worsening and profound RV fibrosis. PP242 reversed pulmonary vascular remodeling and prevented neointimal occlusion of small PAs, significantly reduced PAP and pulmonary vascular resistance, reversed cardiomyocyte hypertrophy and RV remodeling, improved max dP/dT, Ea and RV-AT, and prevented development of RV fibrosis.

Collectively, this data show predominant role of mTORC1 vs. mTORC2 in RV pathology and suggest potential attractiveness of mTOR inhibition to simultaneously target pulmonary vascular remodeling and RV dysfunction in established PH.
 
Rapamycin arteriosclerosis rat study

Effect of sirolimus on arteriosclerosis induced by advanced glycation end products via inhibition of the ILK/mTOR pathway in kidney transplantation recipients.
To investigate the effect and related mechanism of sirolimus (SRL) in arteriosclerosis(AS) induced by advanced glycation end products (AGEs) in kidney transplantation recipients (KTRs).

Human kidney tissues from KTRs before and after treatment with SRL were assessed by hematoxylin-eosin and immunohistochemical staining. Rat vascular smooth muscle cells (VSMCs) were treated with AGEs and/or SRL. The expressions of &#945;-smooth muscle actin (&#945;-SMA), osteopontin (OPN), actinin-associated LIM protein (ALP), proliferating cell nuclear antigen (PCNA), integrin-linked kinase (ILK) and the mTOR signaling pathway proteins were examined using western blot assay. Cytosolic calcium present in VSMCs was also measured by the calcium assay kit and von Kossa staining assay.

The expression of &#945;-SMA was remarkably higher while OPN expression was significantly lower in recipients with AS after they were administered SRL. Rat VSMCs treated with AGEs exhibited significantly lower expression of &#945;-SMA and overexpression of OPN, ALP and PCNA than the other groups.

In contrast, the expression of &#945;-SMA was significantly higher while the expression of OPN, ALP and PCNA was significantly lower in VSMCs treated with both AGEs and SRL. Moreover, the ILK/mTOR signaling pathway was activated in rat VSMCs treated with AGEs, while treatment with AGEs and SRL led to significant inhibition of the ILK/mTOR signaling pathway.

AGEs play a critical role in the development and progression of AS after kidney transplantation, but SRL can reverse these effects and therefore slow down the development of AS through inhibition of the ILK/mTOR signaling pathway.
 
Hi Mopes,

Sorry about the late reply. I was out of the country for a bit.

Thanks for the info on your blood work.

I think I am going to try a low dose of nandrolone decanoate like 50mg/wk on top of my normal trt test dose for a few weeks in the near future.

I am really just interested in the healing properties of the drug, not so much the performance enhancement and hypertrophy aspects. while I am skeptical about unpreventable/irreversible long term adverse effects in humans (I doubt there are any at reasonable doses for reasonable periods of time with proper diet, lifestyle, sleep, bloodwork, ancillaries, etc.), I would rather try to start by finding the minimal effective dose.

I hope your knee is getting better. How is the rehab going?

What are your thoughts on BPC 157 at this point? I'm still waiting for at least one human trial to be published on it. I think one is being conducted now in Mexico for ulcerative colitis or IBS or some other GI issue.
 
Not sure on the bpc, ran it for a couple months, did it help or did I just heal in that period? I have no idea. I'd like to think it helped but I really have no concrete way to say that it did. That said I have no regrets trying it, torn knee is 98% healed but now having the same issues in my good knee (as my doctor said it would as a result of compensation).

Still running the nandrolone, haven't had any joint issues, injury or other long term pain since starting it. Healing properties were what drew me to it as well but now that I'm back hitting the gym hard it's amazing to see what has happened to my strength. Impressive stuff.

Not something I'd stay on forever but been an interesting and timely experiment. Have added in a handful of different supplements for cholesterol support, aged garlic, plant sterols, citrus bergamot, probably a couple others I'm forgetting. Also been taking 2 grams of taurine every night after reading the data which you provided.

Tried a small dose of caber, 0.0625mg twice a week, to drop the prolactin down, helped with my inability to orgasm. I know many say that prolactin can be controlled with proper e2 levels so taking a bit of an AI, maybe .25mg arimidex twice a week, is something I'll also try as an alternative.

I'm not sure 50mg would do anything quite frankly, given the amount of time it'd take to build up in your system I'd think you'd need to give a low dose like that at least 3-4 months to assess any impact.
 
Hi Mopes,

I am happy to hear your first knee injury is 98% better. Sorry to hear about your other knee.

I just came across this study indicated an increase in collagen synthesis in human subjects taking 15g gelatin and 50mg vit c 1 hour before 6 minutes of jump rope 3 x day

m.ajcn.nutrition.org/content/early/2016/11/15/ajcn.116.138594.abstract

Maybe that could help? Worth a try. The vit c was actually in the form of blackcurrant juice. You could get about 50mg vit c from one orange or kiwi.

It's funny to read how some people have amazing healing with BPC157 and others not much at all. I wonder if it is a difference in the quality of the product of different suppliers.

I am not an expert but I believe the BPC157 peptide acetate form, which is commonly sold, is fairly unstable. It is degraded by heat, light, air and shaking. I worked with other peptides for my graduate research and they required extreme care to ensure they were not degraded or destroyed during shipping, storing, reconstituting and administering. Perhaps some or all of the potency of your product was lost somewhere between the time of sequencing and administration.

Glad to hear you are taking taurine with the nandrolone;)

I think you are right 50mg/week may be too low to experience an effect of nandrolone on my pain and injuries. It is just that most of the research shows some pretty good effect in the range of 25-600mg/wk for a variety of conditions, obviously the higher doses have more pronounced effects. That's a huge dose range though, 24 times difference in dose from the low to the high end. In most comparative studies that I have read it looks like nandrolone is about 2.5 times as strong an anabolic as testosterone per mg. So, 50mg nandrolone would be roughly 125mg testosterone in terms of anabolic effect. 125mg increase in test to my trt regimen sound like a lot to me. I am pretty risk aversive. And studies rarely examine the effect the nandrolone + test combo. If I were to take nandrolone, I would have access to comes in 50mg/ml ampules. for convenience, to reduce cost and chance of adverse events I want to start at the low end and work my way. If 50 works I am happy to keep my dose low and cycle it. If it doesn't the next cycle I will bump it up to 100, then if necessary in future cycle 150 and even 200.

I tend to favor the idea of not adding in any drugs unnecessarily. If you are taking a lot of AAS you may need the extra estrogen. Your body is pretty darn good at maintain homeostasis. There may be a number of benefits to estrogen increasing in proportion to test. If you are not having symptoms why take arimidex? as far as I know estrogen is good for HDL and it's a pretty potent anabolics in it's own right.

If I had to take something i like aromasin (exemastane) like. This is a nice exemestane pharmacokinetics study conducted in young healthy males. You won't find many of these with male subjects for other estrogen management drugs.

https://academic.oup.com/jcem/artic...Pharmacokinetics-and-Dose-Finding-of-a-Potent

Thanks for sharing all your experience and info.

All the best.
 
Any new info on nandrolone? Was looking to add 100 mg weekly along with my trt dose of 100 mg test a week…. Goal is lean gains, minimum androgenic sides, but also focus on longevity.
 

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