So browsing the net i found an article ( https://www.pedsr.com/health/selectivity-of-sarms-and-pathological-left-ventricular-hypertro ) which talks about an impact of AAS on the heart.
Now we obviously all know about indirect negative effects on the cardiovascular system such as hypertension, increase in hematocrit, dislipidemia (lowering of hdl and increasing ldl) etc,
However, it is not talked a lot about the direct effects of aas on the androgen receptors in the heart.
Bascially article touches on whether SARMs, while they still do cause some of the same side effects like steroids, dislipidemia namely, attach themselves to the heart causing hypertrophy and fibrosis?
What is interesting is that a study is linked which says that heart contains androgen receptors which only dht bonds to, and not testosterone!
(If the link doesnt work take a look in the first link, original study, study on dht receptors in the heart is listed there)
This is new to me because i thought all androgens eventually attach to all androgen receptors, and only that their affinity differs. It seems it is not the case.
Could it be that steroids like trestolone and perhaps even trenbolone (https://www.ncbi.nlm.nih.gov/pubmed/26584015 ) cause less DIRECT damage to the heart than steroids that convert to dht and dht derivatives?
Quoting from the above study on trenbolone:
"However, only TREN protected against visceral fat accumulation, hypertriglyceridaemia, and hyperinsulinaemia and reduced myocardial damage relative to CTRLs. TEST caused widespread cardiac fibrosis and prostate hyperplasia, which were less pronounced with TREN. We propose that TEST replacement therapy may have contraindications for males with TD and obesity-related MetS. TREN treatment may be more effective in restoring androgen status and reducing cardiovascular risk in males with TD and MetS."
However, lets not forget about trenbolone's neurotoxic effects which prohibits it as an alternative for long term use. But, that is not the subject of this thread.
Could this (tren causing less cardiac fibrosis than test)be because trenbolone is not a substrate for 5 alpha reductase?
It should go the same for other steroids which are uncapable of reducing, such as trestolone.
Anecdotally some people have also said that trestolone was milder on their lipids. And we also know how detrimental dht's are to the lipids.
So what are your thoughts on this?
The main points i want to touch on are:
1)The fact that heart contains receptor for dht and not test and whether steroids that dont undergo 5 alpha reduction are in fact more forgiving to the heart when it comes to the direct stimulation of androgen receptors in the myocytes?
And are we doing more damage to the heart by doing high doses of testosterone and dht derivatives? And should we choose non 5-alpha reducible steroids and sarms instead?
Of course dht is needed but physiologic, replacement dose of test is always a base, so that is not an issue.
2)Heart is a muscle. Do SARMs differentiate between skeletal muscles and cardiac androgen receptors?
Definitely a very interesting subject, and something everyone who is going to inject substances long term whould consider.
edit: Also a major thing to consider is that all the peripheral issues that aas cause like dislipidemia, increase in rbc etc can be somewhat managed by our actions.
However we cant prevent binding of androgens to the receptors in cardiac tissue. I hypothesized about a substance, behaving like a serm does to estrogen, blocking its effects, but this substance would attach itself to the heart and prevent androgens from binding.
Unfortunately afaik no such substance exists yet.
Now we obviously all know about indirect negative effects on the cardiovascular system such as hypertension, increase in hematocrit, dislipidemia (lowering of hdl and increasing ldl) etc,
However, it is not talked a lot about the direct effects of aas on the androgen receptors in the heart.
Bascially article touches on whether SARMs, while they still do cause some of the same side effects like steroids, dislipidemia namely, attach themselves to the heart causing hypertrophy and fibrosis?
What is interesting is that a study is linked which says that heart contains androgen receptors which only dht bonds to, and not testosterone!
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(If the link doesnt work take a look in the first link, original study, study on dht receptors in the heart is listed there)
This is new to me because i thought all androgens eventually attach to all androgen receptors, and only that their affinity differs. It seems it is not the case.
Could it be that steroids like trestolone and perhaps even trenbolone (https://www.ncbi.nlm.nih.gov/pubmed/26584015 ) cause less DIRECT damage to the heart than steroids that convert to dht and dht derivatives?
Quoting from the above study on trenbolone:
"However, only TREN protected against visceral fat accumulation, hypertriglyceridaemia, and hyperinsulinaemia and reduced myocardial damage relative to CTRLs. TEST caused widespread cardiac fibrosis and prostate hyperplasia, which were less pronounced with TREN. We propose that TEST replacement therapy may have contraindications for males with TD and obesity-related MetS. TREN treatment may be more effective in restoring androgen status and reducing cardiovascular risk in males with TD and MetS."
However, lets not forget about trenbolone's neurotoxic effects which prohibits it as an alternative for long term use. But, that is not the subject of this thread.
Could this (tren causing less cardiac fibrosis than test)be because trenbolone is not a substrate for 5 alpha reductase?
It should go the same for other steroids which are uncapable of reducing, such as trestolone.
Anecdotally some people have also said that trestolone was milder on their lipids. And we also know how detrimental dht's are to the lipids.
So what are your thoughts on this?
The main points i want to touch on are:
1)The fact that heart contains receptor for dht and not test and whether steroids that dont undergo 5 alpha reduction are in fact more forgiving to the heart when it comes to the direct stimulation of androgen receptors in the myocytes?
And are we doing more damage to the heart by doing high doses of testosterone and dht derivatives? And should we choose non 5-alpha reducible steroids and sarms instead?
Of course dht is needed but physiologic, replacement dose of test is always a base, so that is not an issue.
2)Heart is a muscle. Do SARMs differentiate between skeletal muscles and cardiac androgen receptors?
Definitely a very interesting subject, and something everyone who is going to inject substances long term whould consider.
edit: Also a major thing to consider is that all the peripheral issues that aas cause like dislipidemia, increase in rbc etc can be somewhat managed by our actions.
However we cant prevent binding of androgens to the receptors in cardiac tissue. I hypothesized about a substance, behaving like a serm does to estrogen, blocking its effects, but this substance would attach itself to the heart and prevent androgens from binding.
Unfortunately afaik no such substance exists yet.
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