Left Ventricle Hypertrophy and Nandrolone ( Decadurabolin )

[tdb]

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.

 

[mopes]

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.

 

[Nelson Vergel]

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

 

[mopes]

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?

 

[SoCal Guy]

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.

 

[SoCal Guy]

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.

 

[SoCal Guy]

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.

 

[tdb]

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.

 

[mopes]

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.

 

[tdb]

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.