Left Ventricle Hypertrophy and Nandrolone ( Decadurabolin )

[tdb]

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.


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-adrenorecptors 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 speculate 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 which rarely seems to be considered by the researchers when examining the subjects' hearts. Considering the millions of AAS users worldwide, these very few case study subjects with heart problems seem to be the exception rather than the rule 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).

 

[Nelson Vergel]

tdb

Great post! You have done your homework. I hope you stick around ExcelMale since we need more people who like digging into scientific references.

My answers:

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

NV: I agree. Most athletes that do not use testosterone or nandrolone have LVH. Anything that makes us use our hearts more would make LVH increase. Heart is muscle and, like any muscle, it can grow with exercise alone. In most cases, this is non-pathological and has little clinical significance provided your blood pressure and cardiovascular parameters are OK. I also suggest to every man on ExcelMale to get a yearly physical with an EKQ as a basic heart test.

The Heart of Trained Athletes


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?


NV: I see no harm if you control those parameters. Your dose is conservatively low anyway. I also assume you are under the care of an educated physician.
Read this information about nandrolone from other posts:

All About Nandrolone

The main concern I have about the use of nandrolone, oxandrolone or higher dose TRT is the reduction of HDL. Unlike high hematocrit, increasing HDL is not as easy.

Just monitor your lipids. Some get good results with 500-1000 mg /day Niacin, citrus bergamot, and others.

Supplements that lower LDL cholesterol and triglycerides and increase HDL.


Finally, do you believe the use of low intensity endurance exercise,

NV: Yes. I use medium weights and use mindful exercise with emphasis on slow concentric movements.

I have a few videos here: Exercise Tips to Lose Fat and Gain Muscle


diet,

NV: Clean nutrition for health, muscle gain and fat loss.


or supplementation with coq10 or d-ribose

NV: See post above on supplements. I love Coq10 also:

Peter Langsjoen, MD discusses why we should take Coenzyme Q10


could be of benefit in preventing any potential unwanted cardiac effects, if one were to cycle nandrolone in the above stated manner?

NV: I think so.

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

NV: Good protocol used by several people on ExcelMale. I have never used the phenylpropionate ester, though. Remember that once you stop that cycle your testosterone will be shut down, so I am assuming you will stay on TRT.

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

 

[MikeXL]

What about the possibility that nandrolone can increase artery calcification?

 

[tdb]

Hi Nelson,

Thanks for the speedy reply! The links are helpful.

In regards to your comment on HDL. I agree it should be monitored and it is probably one of the most difficult factors to manage when using AAS.

You may find this article interesting. I am not yet allowed to attach links so I will just copy and paste below first the article title and then the most pertinent excerpts. I think the article raises (at least) three major points of interest.

1) HDL may be most influenced by the dose and route of administration of the AAS.

2) The association between HDL number and CVD risk is questionable.

3) Testosterone may have beneficial effects on HDL function and particle size that are not necessarily reflected in the number of HDL. And who knows, this may generalize to other AAS or perhaps testosterone in conjunction with other AAS may help to mitigate the potentially deleterious effects of other AAS (pure speculation on my part)

Here is the article title and excerpt:

Testosterone, HDL and cardiovascular risk in men: the jury is still out

Direct evidence for the HDL-C-lowering effect of testosterone derives principally from observations of men using androgenic-anabolic steroids for athletic enhancement [3]. This effect has been achieved consistently with the administration of supraphysiologic doses of oral androgens to young men [2], but has been far less consistent when testosterone therapy has been used at physiologic doses to restore eugonadal serum levels, particularly in older men [4,5]. Moreover, the lipid-related effects of exogenous testosterone appear highly contingent on whether parenteral or oral routes of administration are employed. Oral testosterone administration significantly reduced HDL-C levels in young, healthy men [6], whereas when older, hypogonadal men were treated with transdermal testosterone, we found no significant changes in HDL-C after 3 months of therapy [5]. These disparate effects may be a consequence, in part, of first-pass hepatic metabolism that occurs with oral but not parenteral administration. In addition, the HDL-C-lowering effect of testosterone may be offset, at least partially, by aromatase-mediated conversion of testosterone to estradiol, as estradiol can raise HDL-C levels in men [7], and coadministration of intramuscular testosterone with an aromatase inhibitor led to significant decreases in HDL-C [8]. Increased adiposity and associated aromatase activity in older men could thus play a mitigating role in the androgen-mediated reductions in HDL-C seen in this population. Accordingly, more clinical studies are necessary in order to better define those populations of men at greatest risk of lipid-related effects of testosterone therapy and to determine the testosterone regimens that are least likely to confer seemingly adverse changes in lipid profiles.

Even when reductions in HDL-C are observed as a consequence of androgen therapy, the implications for cardio vascular risk modification remain highly uncertain [2]. Whereas an inverse relationship between HDL-C levels and cardio vascular risk has been demonstrated clearly on a population basis [9], the utility of HDL-C as a biomarker of individual cardio vascular risk has increasingly fallen into question. Underscoring the limitations of assessing HDL-C alone, recent clinical trials have found no decrease in cardiovascular event rate despite significant and substantial increments in HDL-C after treatment intervention in subjects with pre-existing CVD; indeed, the CETP inhibitor torcetrapib raised HDL-C levels by 72% but was associated with an increased rate of cardio vascular events [10]. Conversely, no long-term data have established that the reduced HDL-C levels observed in men receiving testosterone lead to an increased incidence of CVD. Rather, clinical data strongly suggest that men with low circulating levels of testosterone are at greater risk of CVD [11]. These apparently discrepant findings regarding HDL-C and CVD risk may eventually be resolved as the complexity of HDL biology becomes better understood. Currently, research efforts are expanding to incorporate alternative metrics of HDL composition and function, such that HDL-C content is incorporated into a larger context of particle protein, triglyceride and phospholipid content, as well as quantitative measures of HDL's pleiotropic functions.

“The development of new methods to examine the variable composition of HDL therefore promises to offer more nuanced insights into HDL biology overall and, specifically, into the undoubtedly intricate relationships between circulating androgens and HDL composition and function.”

A primary role of HDL-C is that of reverse cholesterol transport, the process whereby HDL particles accept cholesterol from peripheral tissues and transport it to the liver for excretion in bile. These peripheral cholesterol donors include lipid-laden macrophages, which may otherwise deposit cholesterol in the artery wall and contribute to atherogenesis. Rader, Rothblat and colleagues have developed an assay that measures the capacity of serum HDL to efflux cholesterol from macrophages and demonstrated reduced efflux capacity in patients with existing coronary artery disease [12]. Furthermore, investigators found marked interindividual variation in HDL-mediated efflux among subjects with identical HDL-C levels, underscoring the potential dissociation between HDL-C and HDL function [13]. As in vitro data suggest mechanisms by which testosterone could accelerate reverse cholesterol transport [14], a lower HDL-C level could reflect altered kinetics of cholesterol transport that would actually reduce cardio vascular risk. Thus, these data illustrate the difficulty of drawing inferences about HDL function on the basis of HDL-C alone.

“...the role of testosterone in modifying lipoprotein function and cardiovascular risk in men remains highly uncertain and constitutes an intriguing area of emergent research.”

Ongoing research efforts are similarly exploring alternative strategies for assessing the relationship between HDL and CVD, including measurement of HDL particle number and size, determination of HDL protein cargo and assays of other HDL functions [5,15]. For example, our research has generated the novel finding that testosterone replacement in older, hypogonadal men confers changes in the protein composition of HDL particles in the absence of changes in HDL-C [5]. Although we did not observe attendant changes in HDL-cholesterol-efflux capacity, HDL particles also mediate lipid peroxidation, endothelial cell nitric oxide production and immunomodulatory functions [15,16]. The develop ment of new methods to examine the variable composition of HDL therefore promises to offer more nuanced insights into HDL biology overall and, specifically, into the undoubtedly intricate relationships between circulating androgens and HDL composition and function.

In contrast to the historical concern that testosterone might increase cardiovascular risk in men, mounting data now demonstrate elevated risk to be associated with low androgen states [17,18]. This elevated risk is strikingly prominent among men who have undergone androgen-deprivation therapy (ADT) for treatment of prostate cancer, as these men exhibit a two- to three-fold higher incidence of stroke and myocardial infarction, as well as an increased risk of cardiovascular-related mortality after ADT exposures as brief as 6 months [19]. Furthermore, this elevated risk is manifested despite the inconsistent but not infrequent observation of increased HDL-C levels with ADT [19]. However, intervention trials have yielded inconsistent findings. In one study of frail, elderly men, those who received testosterone replacement experienced significantly more cardiovascular events despite gains in mobility and strength [20]. Nonetheless, no increased cardiovascular risk was evident in a similarly designed trial [1]. These conflicting data thus highlight the importance of extending our focus beyond a single HDL-associated metric in order to understand the full scope of testosterone's effects on HDL and the associated implications for cardiovascular risk. In addition, analogous to the Women's Health Initiative, large-scale clinical studies in men are needed to help define specific populations of men who are most likely to benefit from replacement therapy and, further, to establish optimal parameters for the timing, dose and duration of testosterone treatment. As yet, however, the role of testosterone in modifying lipoprotein function and cardiovascular risk in men remains highly uncertain and constitutes an intriguing area of emergent research.

Go to:
Acknowledgments
Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.

 

[tdb]

Yes, I agree with you that HDL can be difficult to manage and should be monitored.

Here is a study using human subjects that looked directly at the effect of 100mg/wk x 6 wks of nandrolone on blood lipids and found no effect!

I cannot attach links so I will copy and paste below:

Lack of demonstrated effect of nandrolone on serum lipids

Abstract
Numerous prior studies of serum lipid levels during anabolic steroid (AS) use have uniformly demonstrated dramatic adverse lipid profiles (eg, average high-density lipoprotein [HDL] depression of 50%) during administration of 17α-alkylated AS. In contrast, the existing studies of 17β-esterified AS have shown mild or absent lipid effects (eg, HDL depression 0% to 16%) with these agents. Thus, the potential effects on serum lipids of individual AS are an important clinical consideration. The present study was therefore designed to investigate the lipid effects of nandrolone, a 17β-esterified AS. Twenty-one men and three women had lipid profiles measured before and after administration of nandrolone decanoate 100 mg intramuscularly (IM) once a week for 6 weeks. No significant change was noted in HDL cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol, triglycerides, the total cholesterol to HDL-C ratio, or the ratio from nandrolone treatment. Moreover, observed trends toward HDL-C depression (−2.00 ± 8.83 mg/dL; values reported are for men only unless noted otherwise) and LDL elevation (+5.05 ± 20.45 mg/dL) were small. In power analysis, HDL-C depressions of 6.3, 7.6, or 8.7 mg/dL during nandrolone were ruled out with powers of 80%, 95%, and 99%, respectively.

 

[Nelson Vergel]

MikeXL:

There is no human data on nandrolone and calcium scores.

tdb:

We can debate the role of HDL's quantity and particle size in cardiovascular events but , as I said before, it pays to be safe and to monitor and manage your lipids. Short term cycles should not be a huge concern, but long term exposure definitely requires monitoring. The problem is that most men using androgens beyond testosterone are not doing so under physician's monitoring.

 

[tdb]

Hi Nelson,

I agree with you completely. These are serious drugs that should not be used in a cavalier manner. Androgen use should be done under the care of a physician and lipids should be a part of regular blood work.

I am still researching and considering 100mg * 8 weeks nandrolone with my regular TRT dose for joint and tendon issues.

Do you have any other suggestions for joints and tendons?

Thanks and happy New Year!

 

[Nelson Vergel]

tdb

Some guys report good results with two doses per day of collagen. I am not sure if the effect is due to "placebo effect".

Great Lakes Gelatin, Paleo Collagen Hydrolysate, Collagen Peptides

 

[SoCal Guy]

The athletic version is not necessarily harmless. It depends on how over-size your ventricle actually is, not whether the cause was steroids or uncontrolled hypertension.

The reason is basic physics -- the extra muscle actually reduces ejection fraction, because the heart is a round muscle. Therefore as the heart gets more muscular, its diameter increases -- which reduces the amount of pumping pressure it can deliver. (Just as you can squeeze a tangerine harder than you can squeeze a basketball.) So the more muscular the heart, the weaker the pumping. Worse, this effect can become a negative runaway -- the heart adds muscle to keep the pressure up -- which increases diameter, lowering pressure.

So you want to reverse significant enlargement if at all possible (successful reversal is called "reverse remodeling" of the ventricle.)

You will find no shortage of doctors, even cardiologists, who will tell you that LVH is irreversible, but the newest research is that adequate (high enough) doses of a newer beta blocker called carvedilol (Coreg) 2x/day can reverse much of it.

The reason carvedilol can do this where other beta blockers couldn't is coreg is one of the rare beta blockers that also reduces constriction in your veins and arteries. This reduces the 'back pressure' the heart contends with, so less force is needed to keep you oxygenated. So the ventricle is finally deloaded and the excess muscle mass can gradually revert toward normal. In some cases, almost complete reverse remodeling has been seen with similar restoration of ejection fraction.

Hit pubmed for endless cites, but here are a few good ones:

25mg/day carvedilol reverses dilated cardiac myopathy

administration instructions
more info

almost normal ejection fraction after 15 years at 50mg/day

another good result after 22 days at 50mg/day

Oh, one last thing -- carvedilol IMPROVES insulin resistance, whereas other beta blockers like metoprolol WORSEN it.

It's a pretty amazing drug.

 

[Nelson Vergel]

I would rather use an ACE or ARB to prevent or reverse LVH since beta blockers are known for decreasing sex drive and penis sensitivity. I take losartan.

Effects of Losartan on Left Ventricular Hypertrophy and Fibrosis in Patients With Nonobstructive Hypertrophic Cardiomyopathy

Another potential benefit of losartan:

Can Losartan decrease high hematocrit caused by testosterone replacement?
Here are some more posts on LVH

Heart issues 10 years in (Left Ventricle Hypertrophy)


Rejected from blood donation because of white coat syndrome...


LVH and cardiomyopathy confirmed. Do I need to stop my Test/hgh ...

Thread: Feedback Please on HCG Protocol and Labs....


Does anyone use Nandrolone (Deca Durabolin) ? [Archive ...


High hemocrit possible solution? study on Tumeric Curcumin

 

[SoCal Guy]

I would rather use an ACE or ARB to prevent or reverse LVH since beta blockers are known for decreasing sex drive and penis sensitivity. I take losartan.

Thanks for the losartan info. I'm already on that as well, but it's nice to know that it also helps.

FWIW, I haven't had an issue with drive or sensitivity on either the carvedilol, or the metoprolol before.

 

[tdb]

Hi Nelson,

Thank you for your suggestion.

I have been taking that exact product along with several other joint support supplements such as glucosamine, msm, fermented cod liver oil, d3, magnesium, and vit c (rarely at 500mg), turmeric, apple cider vinegar, raw honey, and a diet rich in sulfurs, bone broths, collagen, organ meats of all kinds, lots of green veggies, no processed foods, when I eat out it is sushi. I only drink water and rarely lime water, watermelon juice, rooibos tea, turmeic tea. I get plenty of sunshine, sleep 9 hours every night, walk 1 hour each day, resistant train 3-4 days a week light weight, higher volume, relatively slow reps, river swim all year long at a national park (pristine water) 3-4 days a week, prehab/rehab work 2-3 days a week. Everything is on point which is why I find my accumulating joint and tendon issues both baffling and frustrating.

I have accumulated both chronic and accute sports injuries from boxing and surfing as well as a nasty motorcycle accident a few years ago. I have seen several docs and physiotherapist, Chinese medicine doctors, acupuncturists, massage therapists, etc. I have not been diagnosed with any disease like arthritis. When I was diagnosed with primary hypogonadism and prescribed testosterone I saw a lot of improvements but not so much in my joints and tendons. It is only because I fel like I have exhausted other options that I have started to explore drugs like nandrolone. I am still young, early thirties. I want to continue to be active, healthy and happy for myself and my newborn son for many years to come.

My current endocrinologist is very cooperative and if I present him with the scientific literature to support my position, he will evaluate it, we will discuss it and then develop a plan of action that we are both comfortable with. So, I expect his compliance if I should want to try nandrolone for a short course.

SoCal Guy

Thank you for your links on carvediol.

 

[GA8314]

The athletic version is not necessarily harmless. It depends on how over-size your ventricle actually is, not whether the cause was steroids or uncontrolled hypertension.

The reason is basic physics -- the extra muscle actually reduces ejection fraction, because the heart is a round muscle. Therefore as the heart gets more muscular, its diameter increases -- which reduces the amount of pumping pressure it can deliver. (Just as you can squeeze a tangerine harder than you can squeeze a basketball.) So the more muscular the heart, the weaker the pumping. Worse, this effect can become a negative runaway -- the heart adds muscle to keep the pressure up -- which increases diameter, lowering pressure.

So you want to reverse significant enlargement if at all possible (successful reversal is called "reverse remodeling" of the ventricle.)

You will find no shortage of doctors, even cardiologists, who will tell you that LVH is irreversible, but the newest research is that adequate (high enough) doses of a newer beta blocker called carvedilol (Coreg) 2x/day can reverse much of it.

The reason carvedilol can do this where other beta blockers couldn't is coreg is one of the rare beta blockers that also reduces constriction in your veins and arteries. This reduces the 'back pressure' the heart contends with, so less force is needed to keep you oxygenated. So the ventricle is finally deloaded and the excess muscle mass can gradually revert toward normal. In some cases, almost complete reverse remodeling has been seen with similar restoration of ejection fraction.

Hit pubmed for endless cites, but here are a few good ones:

25mg/day carvedilol reverses dilated cardiac myopathy

administration instructions
more info

almost normal ejection fraction after 15 years at 50mg/day

another good result after 22 days at 50mg/day

Oh, one last thing -- carvedilol IMPROVES insulin resistance, whereas other beta blockers like metoprolol WORSEN it.

It's a pretty amazing drug.

Nice post. One caveat is that reversal of DILATED cardiomyopathy may be different from concentric cardiomyopathy. Dilated cardiomyopathy is from traditional heart failure and is eccentric in nature. LVH is concentric hypertrophy.

I was unaware that carvedilol IMPROVES insulin sensitivity, but when compared to atenolol and metoprolol I am aware that it did not DECREASE insulin sensitivity. Interestingly, Nebivolol is also an interesting BB. Not sure about literature relative to it's effects on cardiac remodeling, but it also does not increase insulin resistance, AND (and this seems unique to Nebivolol) it also vasodilates via a unique N02 releasing mechanism, and thus has not shown to produce ED, as most all other BB's can indeed (including carvedilol).

I've taken most types of BB's and the thing I don't like about carvedilol is because of it's alpha1 blocking activity, it can give you a bit of a stuffy nose. Nebivolol does not do that as much, or at all really.

Also, Nebivolol, in doses of 5mg and less, does not seem to inhibit some rate increase in response to exercise, so guys report less fatigue on Nebivolol.

Anyway, good discussion.

 

[mopes]

My current endocrinologist is very cooperative and if I present him with the scientific literature to support my position, he will evaluate it, we will discuss it and then develop a plan of action that we are both comfortable with. So, I expect his compliance if I should want to try nandrolone for a short course.

Curious what you ended up doing with regards to nandrolone and/or where your research lead you.

 

[tdb]

Hi Mopes,

Thanks for your interest. I am still researching other options. Namely, HGH, BPC-157, and stanozolol.

The only real concern I have with Nandrolone at this point is prolactin. On my last bloodwork my prolactin was a couple points above the normal reference range. My doctor didn't seem worried but I don't want to exacerbate my high prolactin if there are other better options.

Do you have any suggestions?

Thanks.

 

[mopes]

I'm in a similar boat to you. Mid/late 30s w number of injuries accumulated over the years. Most recently I partially tore my MCL skiing.

Been running between 250-500 mcg of bpc 157 daily into the knee for the past four weeks along with 4mg tb500 weekly (split in two doses).

Also started 210mg of nandrolone weekly and bumped my t cyp dosage to 210mg weekly to match. Injection schedule is EOD.

Joint pain is down dramatically and knee is it a level docs indicated would take twice as long as it has. Just dropped the bpc and tb500 but will stay on the nandrolone for now. Unclear how long I will run it as I am in this for the long haul and still have concerns over LVH/impact on heart. The research continues...

 

[tdb]

Yeah Mopes we are definitely in the same boat!

Your test/nandrolone doses are very similar to what I am considering trying.

Have you had any blood work done while on these meds? I would love to see.

Are you taking anything for estrogen management?

As far as concerns over Left ventricle hypertrophy, according to this paper 200mg/wk for 8 weeks had no influence on heart structure or function in human males. So maybe short cycles is the way to go?:

https://www.researchgate.net/profil...ructure-and-function-in-strength-athletes.pdf


I came across some other papers that I think you will find to be useful. I will ist them below. The bottom line appears to be that one should supplement with taurine when taking nandrolone:

1) Impact of taurine on rats given nandrolone:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4932817/?report=classic

2) Amelioration of nandrolone induced testicular and sperm toxicity by taurine

https://www.researchgate.net/profil...ic_Pathway/links/56686f5808ae7dc22ad36c9a.pdf

3) Taurine helps to ameliorate the hypercoagulable blood of nandrolone users4)

https://www.ncbi.nlm.nih.gov/pubmed/23160242

4)Increase platelet aggregatin induced by nandrolone use is lessened by taurine supplementation

http://www.acta-endo.ro/archive/abstract?doi=2013.33

 

[mopes]

Thanks for the links. Good info on the taurine will dig into it more. I'm out of the country for two weeks but will be running bloods when I get back.

Mostly concerned about my hdl so will be interesting to see how that looks. Been taking 500mg of citrus bergamot twice a day with some coq10. Will add some plant sterols after bloodwork if need be.

Not sure 8 weeks is long enough to run nandrolone given the extremely long half life and amount of time it takes to build up in the system. I can say that personally I didn't feel a thing until four weeks in but now certainly notice strength increase and my joints feel far better than they have in years...

 

[tdb]

Hi Mopes,

Good point about the decanoate ester. For 8 week cycle, perhaps Nandrolone Phenylpropionate (NPP) would be more appropriate?

I would love to see your bloodwork when you get it done. I am interested in prolactin and estrogen levels.

Have you noticed any adverse effects from your current regimen?

Glad to hear you are feeling well. That gives me a lot of hope!

Be well.

 

[mopes]

I haven't noticed any adverse effects, feel fantastic. I'm not running an AI (I've dosed 6.25 mg aromasin once or twice as an experiment). I'm also on 1000iu hcg twice a week. Thought I would get some high estrogen sides, acne, etc but have not.

Libido is very strong (stronger than on t alone) but erection quality is down a bit the last couple weeks, I realize this could be estrogen or prolactin related so will be interesting to see what bloods look like vs my baseline numbers. Idea of taking caber or prami does not appeal to me one bit as daws is nothing to take lightly. May try bumping t up to 250 after bloods and see if a slightly higher dose offsets what I assume is deca ****...