Direct effects of AAS and SARMs on the heart

CroLifter

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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.
 
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CroLifter

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This study (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2613982/) says how mesterolone (proviron) induces cardiac hypertrophy.

now we all know that proviron is inactivated in muscle tissue, like dht.
This would point in the direction that really it is the dht that contributes to heart hypertrophy.

Now proviron is considered to have weaker binding affinity than testosterone. Even though it has weaker binding affinity, it directly stimulates cardiac hypertropfy.

If proviron, which has lower binding affinity than testpsterone for the AR, yet induces cardiac hypertrophy like dht but unlike T, could that mean that cardiac androgen receptors are senisitive to dht not because of its higher binding affinity for the receptor but because of the structural difference between dht and testosterone?

also very interesting to me is the study on trenbolone which states less cardiac remodelling than testosterone because tren is more "selective" towards skeletal muscle.

also, testosterone induced more bone mineralization than tren, and we know that dht is strong androgen in bone tissue.

and yet tren has such a higher binding affinity for the AR than testosterone, and yet testosterone is more potent at bone mineralization and maintaining prostate mass. So it might not be all about binding affinity, but perhaps the structure of the molecule itself? Even though that might be the same thing (structure of the molecule dictates binding affinity? But different structures have different binding affinities in various tissues? Hence SARMS are possible?)
 
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Joshinator

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Nandrolone causes left ventricular hypertrophy, its not a DHT
 

CroLifter

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Nandrolone causes left ventricular hypertrophy, its not a DHT
I am not claiming that dht is the only hormone that causes this it would be logical thay all aas do this as they attach to the ARs.
Regarding nandrolone: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4576214/

by looking at the graphs i dont see any measurable difference between exercise groups and exercise+nandrolone when it comes to hypertrophy.
however nandrolone + exercise has the most incident of ventricular fibrillation.
Vigorous long term exercise itself leads to a higher incidence of arrhytmias: https://www.ncbi.nlm.nih.gov/pubmed/11863350
 
Iwilleattuna

Iwilleattuna

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Finasteride and other anti androgens reducing androgens actually increases heart failure risk because the heart needs androgens to function especially the male heart. On one forum, a dude apparently had heart failure(but lived) from ru58841.
 

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