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-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).
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-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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