Primo: risk-reward profile... is it 'conspicuous consumption' or does it really only 'shine' with long-term use?

[Jin23]

It's the fact you keep returning to blood work and an EKG that is the reason you are healthy.

Idk how long you have been blasting and I guess maybe because I work in health, I understand that cardiac changes/issues can happen overtime and it goes more than simply blood work.

People have told you in other threads that their EKG seems fine and then all of a sudden they have heart failure. We have told you it goes further past blood work, and I'm not going to go over basic medical knowledge and educate you. You should be doing that on your own.




Jin23 has mentioned a neurological toll on you but have you ever searched up neurologic health markers and if there are any?

You kept. saying "logically" but you have a limited understanding of health markers and you cannot draw a proper conclusion from your actions. It's like solving algebra when you do not understand multiplication.


People have tried to educate you, but you are trying to justify your actions. You kept saying it was "fear of the unknown".

Maybe jin is right and all these androgens over time have fucked your brain.


It's not just us, people in other threads have made comments about your practice but you refuse to listen.

I stopped reading his comments the moment he wrote that androgens don't affect his mental state. But even before he did that, it was obvious that he is so impulsive and adhd like, that it's impossible to talk to him. I also sense a hindrance of borderline personality disorder or some other unstable personality disorder. Just don't fall for his provocations, such people are excellent at it.

There is going to be literally hundreds of similar people on forums, that you're going to come across, as soon as you'll get through to this guy, it's going to be the next guy that you'll have to fight, explain and convince again, and again, ... We're not paid to do this.

He should have started the conversation like: "This is my reasoning, but if y'all are willing to fight my logic and scrutinize my writing in a non hostile discourse, I would be really grateful to y'all." But nobody comes off like that. And I'm not fighting anybody for the sake of getting through them, not anymore, I have nothing to gain. Pay me or ask me nicely at the get go, stop writing a gazilion word long posts and stop making a million threads in one day ... I mean why, why would I or anybody else do it? If you're such a god damn smart ass and a manipulator?

Aas cause gene transcription, epigenitc changes, they rew up the whole system, everything from the brain to the gonads. In the broadest of meaning, your biological age is going to skip a few decades, Markers of arterial health could serve as accurate non-invasive predictors of human biological and chronological age, but literally everything can happen. From early onset cognitive decline, dementia, adhd, to aterosclerosis, liver, kindey failure, I mean, every fucking thing is effected. The thing that will kill you is just the weakest link for you personally, it might be the heart, might not be, but it doesn't really matter all that much what will actually kill you, as you can have all sorts of medical problems that wont kill you but your life will revolve around doctors a lot and it's going to be a pita. Death is one thing, but being fucked up, or having multiple diagnosis, that are manageable or just going through the diagnostic procedures, not figuring out what is actually the problem, and suffering in between ... You know, when a smoker says "you got to die from something, either this, or a car might run me over ..." Well, the process of dying from lung cancer can take a decade of battling with the disease, and before that, you can have COPD, which is also a pita, and you and your family are suffering all this time ...

5 iu's of GH a sustainable trt+ approach? Think maybe like 1.5 iu. 200/200 test primo? Think maybe like 1500 ng/dl ... Or 700 ng/dl plus 50mg primo ... I mean really. Dying is a process. And it drags you and everybody else who is closest to you down in to the ground. Just having a spontaneous heart attack which actually results in you being dead and not having half of your face numb, or a brain hemorrhage that doesn't leave your right arm useless and in tremors is a blessing, honestly.

 

[Jin23]

I not new to steroid use, but I'm fairly new to this model of use, because of how I now have access to raws and can brew huge batches for myself. But I never learned much about blood work and other sides to look for other than the bro basics; and when I watch all the YouTubes of pro and videos on gear, all I hear about is how everyone monitors their blood work and heart, and that's really it. So I assumed that's all that really mattered. Of course I do know that many are liver-toxic and things like that, so I learned not to take orals again; it's why I was interested in Victor Black, but I also didn't think it made any sense to cruise or get off unless you're going for long periods of time, not just 6-8 weeks, which TypeIIX chimed in and showed with a study that on needs to be off 2-3x longer than on...so that's what I was looking for, scientific justification to refute my own "logic"; simple as that. So now I see why bodybuilders say, when someone makes the choice to take gear, they know of the risks, and accept those risks as a tradeoff for a life they want to live.

I have PTSD from the war and I am simply challenging something that I'm being told to believe. When provided factual information, I have no choice but to accept what that information is; I'm not trying to start shit with random strangers on a board for fun. I've been very transparent with everything I've done on here, and I may look stupid to many, but that's fine.

So with everything you listed about, then why not be against the use of steroids completely? This is what I don't understand coming from you. You have to clarify what use is acceptable in your opinion, or if any at all.

Again, the things you listed may also not happen to someone, as everyone is different. Now if someone is monitoring their blood and other numerous tests you'd want them to have, and they all come out okay, then why wouldn't they continue? Milos would argue against you, saying proper steroid use is actually healthy, when monitored and not abused. But again, if you think the safest way is to not take anything at all, then that should be your position. But we all chose to do so knowing the risks (or at least some of them) because this is the life we want to live; I argue, it's better to live how you want and die doing something you love, rather than living a life you don't like and dying. Of course, no one needs to take steroids to train in the gym, nor risk dying to do so as well.

What I meant by the androgens not affecting my mood is, they aren't making me irritable or angry, nor have they made me less intelligent or irrational. The only steroid that noticeably affects my mood is tren, where I do get more irritable and its obvious to even my wife. Again, I have PTSD and have a hypervigilance complex; I also have a hard time sticking to one thing as I lose interest in it, or when I'm doing something, I begin to doubt it, which is why I flip-flop a lot. This is not caused by steroids, because I was diagnosed with PTSD from after the war. Could it all be exacerbated by steroids? Possibly. But me asking questions about why people do things isn't a sign of anything but curiosity.

Could I be addicted to steroids? Perhaps. But is it the steroids I'm addicted to, or is it the fear that if I stop I'll lose my progress? Probably the latter.

Damn bro, if there is a group of people to whom I would disadvise the use of androgens is people with anxiety disorders, ptsd, ie. dysregulated hpa aixis, hyperactive amygdala, and with people who have adhd, unstable personality disorders. Androgens kinda make everything in regards to ptsd worse. Unless you're on some proper dosages of ssri's or some other AD's that regulate your fight or flight response system ... But in any case, it's probably really contra productive for you.

Yes, you are adhd. If it's the ptsd causing or were you adhd before that, I have no idea. Anxiety causes adhd but is also caused by adhd. It's was really clear from your writing, but now that you've mentioned it, the "flip floping", that is a typical adhd pathology and it's called "switching" , novelty seeking. It's your brain, desperately looking for dopamine. Look in to it, I guarantee that eventually, you will become much more cognizant and mindful of your behavior and internal processes.

I'm more or less against aas yes. They have very little to offer. But I am mostly against being on cycle all the time. Meaning, high dose cruising and then blasting. It just turns people to thick headed idiots. If you ask me, aas use in terms of cycling, should be limited to 6 to 10 week cutting cycles only. Done maybe once a year max. But, I'm not against banning anything, or telling people what they should or should not do. Imo every drug should be decriminalized. But legalization should be a very slow process, as cultural knowledge is very much needed in order for random teens to not fucking up their whole brain chemistry/life's with 3mmc or some other shit because they weren't educated properly. Same goes with aas. The amount of adhd and cognitive decline we'll see in the future is going to be far more then what we have now.

I'm sorry to hear you've got ptsd and I hope it's not from invading some poor 3rd world countries.

 

[GuerillaPete]

Damn bro, if there is a group of people to whom I would disadvise the use of androgens is people with anxiety disorders, ptsd, ie. dysregulated hpa aixis, hyperactive amygdala, and with people who have adhd, unstable personality disorders. Androgens kinda make everything in regards to ptsd worse. Unless you're on some proper dosages of ssri's or some other AD's that regulate your fight or flight response system ... But in any case, it's probably really contra productive for you.

Yes, you are adhd. If it's the ptsd causing or were you adhd before that, I have no idea. Anxiety causes adhd but is also caused by adhd. It's was really clear from your writing, but now that you've mentioned it, the "flip floping", that is a typical adhd pathology and it's called "switching" , novelty seeking. It's your brain, desperately looking for dopamine. Look in to it, I guarantee that eventually, you will become much more cognizant and mindful of your behavior and internal processes.

I'm more or less against aas yes. They have very little to offer. But I am mostly against being on cycle all the time. Meaning, high dose cruising and then blasting. It just turns people to thick headed idiots. If you ask me, aas use in terms of cycling, should be limited to 6 to 10 week cutting cycles only. Done maybe once a year max. But, I'm not against banning anything, or telling people what they should or should not do. Imo every drug should be decriminalized. But legalization should be a very slow process, as cultural knowledge is very much needed in order for random teens to not fucking up their whole brain chemistry/life's with 3mmc or some other shit because they weren't educated properly. Same goes with aas. The amount of adhd and cognitive decline we'll see in the future is going to be far more then what we have now.

I'm sorry to hear you've got ptsd and I hope it's not from invading some poor 3rd world countries.

I agree he is not fit mentally to run aas and is using them in a self destructive manner .

 

[Type-IIx]

Since you did not post a link to the HARLEM trial data, I cannot check this for myself. The data showed that a 16 week cycle at 9/10 of a gram weekly caused bad changes (e.g., left ventricle mass ↑ by 28.3 g) and diastolic function (e.g., E/A-ratio by T₁ declined -0.45 - no idea what that means!), so ouch. The bad changes were reversed by month 9 of not pinning,

I have a question.

Is that the first time that they checked, or did they check at 3 months, at 6 months, and so on? Did they check earlier than 9 months?

Left ventricle mass - I assume it decreases in tiny amounts over time, not all at once.

E/A-ratio by . . . ok, read a little on Goole, so I have an idea, even if it is not a very good one. Is this something that changes daily in tiny increments, or does it suddenly normalize all at once?

They checked at a single time-point, 1 yr post-initiation of the prior cycle, after total washout. It'd be fantastic to be able to plot more regular incremental changes, but alas, this would be prohibitively expensive and not something that a free society could ever pull off for a load of black market gear users. Both parameters (LV mass & E/A-ratio) surely return to base-line incrementally. And yet, such particularized data does not exist and is unlikely ever to exist. My approach is always going to be to look at the data that we have, rather than let perfect be the enemy of the good.

The data is from
Smit Diederik L., Voogel A. J., Heijer, Martin den, Ronde Willem de. (2021). Anabolic Androgenic Steroids Induce Reversible Left Ventricular Hypertrophy and Cardiac Dysfunction. Echocardiography Results of the HAARLEM Study. Frontiers in Reproductive Health, 3, 58. doi:10.3389/frph.2021.732318

 

[malfeasance]

Thanks, Type-IIx, I just saw your response (the site has been down)

So, looking at the data we have, such as it is, should 9 months off be enough to reverse cardiac maladaptations, even if they have been abusing for years? Or does that study not support that conclusion?

And would 100-150mg weekly of testosterone (somewhere in that range) be "off" for purposes of this discussion, or does a person need to crash his testosterone blood levels down to those of an 11 year old girl? Keeping in mind that a long term user is probably TRT for life (TRT, not cruise).

 

[Type-IIx]

Thanks, Type-IIx, I just saw your response (the site has been down)

So, looking at the data we have, such as it is, should 9 months off be enough to reverse cardiac maladaptations, even if they have been abusing for years? Or does that study not support that conclusion?

And would 100-150mg weekly of testosterone (somewhere in that range) be "off" for purposes of this discussion, or does a person need to crash his testosterone blood levels down to those of an 11 year old girl? Keeping in mind that a long term user is probably TRT for life (TRT, not cruise).

We have to be a bit parsimonious with our interpretation of the data. This trial (HAARLEM) really only supports that AAS dose-dependently induced (but # of AAS used were associated with reduced [arguing for synergistic effects] & orals were associated with greater) cardiac maladaptations on this time-frame that was reversible by ~ 9 mo of cessation.

From my view of data that includes this study, my view is that 9 mo at TRT (true TRT [described below], but perhaps optimistically up to 100 mg weekly T) would be unlikely to completely reverse, but probably still dramatically reduce, say 1 yr of use. Once you start talking about multi-year use, there's not much data to look at besides cadaver/post-mortem data (where you'll see things like testis cell necrosis and the results of toxicity [e.g., irreversible cell death] in all the tissues that these hormones effect).

100 mg weekly T is probably as high as you can go without siginificant cardiac maladaptations (and I am on optimist here). A lot of cardiologists and such get scared by 100+ mg weekly "TRT" scripts and such.

True TRT (according to current clinical therapeutic guidelines) is really 250 mg testosterone enanthate/cypionate administered every 21 days to start, titrated up or down depending on the mid-interval target of 500 - 800 ng/dL (i.e., at 14 days, measure serum TT: increase or decrease dose oriented towards this target).

A principal concern for older guys (I know you mention that this applies to you, so I'd be remiss not to raise any issues here) is the age-related TRT polycythemia (hematocrit > 0.54), that is dose-dependent & related to rapidity of action, i.e., peak blood T concentrations. The issue with rapidity of action/peak blood T arises practically from frequent pinning (even a constant dose), so if you pin 2x weekly that's worse on your hematocrit than pinning every 3 weeks. Sure, you get that 1 large peak, but it's less frequent. The reason AAS guys pin often, aside from the practical matter of only being able to pin so much oil at once, is the effect on strength/gains that we see with peaking blood T.

 

[malfeasance]

testis cell necrosis and the results of toxicity [e.g., irreversible cell death] in all the tissues that these hormones effect

Argh! WTH???

 

[malfeasance]

A principal concern for older guys (I know you mention that this applies to you, so I'd be remiss not to raise any issues here) is the age-related TRT polycythemia (hematocrit > 0.54), that is dose-dependent & related to rapidity of action, i.e., peak blood T concentrations. The issue with rapidity of action/peak blood T arises practically from frequent pinning (even a constant dose), so if you pin 2x weekly that's worse on your hematocrit than pinning every 3 weeks. Sure, you get that 1 large peak, but it's less frequent. The reason AAS guys pin often, aside from the practical matter of only being able to pin so much oil at once, is the effect on strength/gains that we see with peaking blood T.

Well, that gives me something to think about, for sure.

Right now I am Test C twice a week, 3.5 days apart, using an insulin syringe for 100mg a week. My doctor actually preferred I split it up - most of his patients would never consider that because of a dislike of pinning, but I am not going to pretend that my doc is a hormone expert or has reviewed the data you are sharing.

I also check on hemoglobin and hematocrit at least a couple of times a year.

And donate.

But I guess now I need to consider less frequent pinning.

 

[Type-IIx]

Argh! WTH???

If it makes you feel any better, that data is confounded a bit by the fact that all of those guys were polysubstance (street drug) abusers also.

 

[Type-IIx]

Well, that gives me something to think about, for sure.

Right now I am Test C twice a week, 3.5 days apart, using an insulin syringe for 100mg a week. My doctor actually preferred I split it up - most of his patients would never consider that because of a dislike of pinning, but I am not going to pretend that my doc is a hormone expert or has reviewed the data you are sharing.

I also check on hemoglobin and hematocrit at least a couple of times a year.

And donate.

But I guess now I need to consider less frequent pinning.

I mean, he doesn't sounds like a bad doc - a good one even. It's just something to consider if your hematocrit/hemoglobin run high for you (i.e., donation is intolerably frequent).

Interestingly, there's data that even higher frequency (i.e., daily) subcutaneous injections (not using oils intended for deep intramuscular injection, but something like the Xyosted auto-injector preparation, that includes chlorbutanol not benzyl alcohol, for example) are associated with reduced erythropoiesis (the increase to hematocrit) & aromatization. With respect to erythropoesis, it is plausible that smaller daily T injections, resembling physiologic secretion, do not affect hepcidin activity to the same degree that is seen with supra-physiologic T levels from weekly IM injections. With respect to aromatization, It is plausible that reduced blood flow to adipose tissue (vs. skeletal muscle) thereby results in slower release from depot to the liver Esterase to become active, and so depending on an individual's binding hormone (i.e., SHBG, albumin, α₁ acid glycoprotein, corticosteroid binding globulin) profile, this will almost certainly result in reduced Aromatase activity.

 

[nok]

@Type-IIx curious how, and to what degree, telmisartan/lisinopril may deter remodelling of cardiac muscle.

 

[Type-IIx]

@Type-IIx curious how, and to what degree, telmisartan/lisinopril may deter remodelling of cardiac muscle.

A bit off topic, but I'll answer:

AAS-induced left ventricular hypertrophy (LVH) & diastolic dysfunction are qualitatively different from LVH caused by pressure overload, though there may be some partial overlap (that ARBs or ACE inhibitors might to some extent partially ameliorate) in some individuals.

The time-course of AAS-induced cardiac maladaptations is far too rapid to be merely due to anything preventable by these drugs mentioned.

ARBs & ACE inhibitors hook into the RAAS (renin-angiotensin-aldosterone system) & serve to lower aldosterone & angiotensin II, thereby ↓vascoconstriction & ↑water & sodium excretion (↓fluid retention/edema). These drugs, then, reduce pressure-induced cardiac maladaptations.

Estrogens regulate fluid balance in large part via RAAS action, primarily by acting on aldosterone & on the CNS, regulating thirst, fluid, and sodium intake. This is why AIs ameliorate fluid retention as well as hypertension in users with very high estrogen levels.

In some individuals, androgens do seem to provoke RAAS-mediated pressure overload – but not all. Ibuprofen is a prostaglandin (PG) inhibitor that completely blocks RAAS activity, and would seem a more appropriate selection of compound based on its tolerability vs. ACE inhibitors & ARBs.

But AAS users that never even become chronically hypertensive should never use these drugs "prophylactically" because the risks far outweigh the benefits.

Besides any pressure-induced LVH, AAS have direct effects on cardiomyocytes, electrolyte channels and their associated proteins of these cardiac cells, shift the redox balance towards more oxidative stress, change the ionotropic response to adrenergic activity, etc.

And then GH (as rhGH) has yet further effects, inducing LVH & cardiac maladaptations, probably even acting synergistically (1 + 1 > 2) with AAS in these effects.

 

[Jin23]

A bit off topic, but I'll answer:

AAS-induced left ventricular hypertrophy (LVH) & diastolic dysfunction are qualitatively different from LVH caused by pressure overload, though there may be some partial overlap (that ARBs or ACE inhibitors might to some extent partially ameliorate) in some individuals.

The time-course of AAS-induced cardiac maladaptations is far too rapid to be merely due to anything preventable by these drugs mentioned.

ARBs & ACE inhibitors hook into the RAAS (renin-angiotensin-aldosterone system) & serve to lower aldosterone & angiotensin II, thereby ↓vascoconstriction & ↑water & sodium excretion (↓fluid retention/edema). These drugs, then, reduce pressure-induced cardiac maladaptations.

Estrogens regulate fluid balance in large part via RAAS action, primarily by acting on aldosterone & on the CNS, regulating thirst, fluid, and sodium intake. This is why AIs ameliorate fluid retention as well as hypertension in users with very high estrogen levels.

In some individuals, androgens do seem to provoke RAAS-mediated pressure overload – but not all. Ibuprofen is a prostaglandin (PG) inhibitor that completely blocks RAAS activity, and would seem a more appropriate selection of compound based on its tolerability vs. ACE inhibitors & ARBs.

But AAS users that never even become chronically hypertensive should never use these drugs "prophylactically" because the risks far outweigh the benefits.

Besides any pressure-induced LVH, AAS have direct effects on cardiomyocytes, electrolyte channels and their associated proteins of these cardiac cells, shift the redox balance towards more oxidative stress, change the ionotropic response to adrenergic activity, etc.

And then GH (as rhGH) has yet further effects, inducing LVH & cardiac maladaptations, probably even acting synergistically (1 + 1 > 2) with AAS in these effects.

This post deserves a bump.

*Didn't know aas change alpha/beta receptor expression and sensitivity. That's a good catch!

 

[Inspired]

This post deserves a bump.

*Didn't know aas change alpha/beta receptor expression and sensitivity. That's a good catch!

Well, it's common sense but are adrenergic effects really always a bad thing/contributor to AAS induced negative cardiac remodeling? I'm going to bet that controlling the pressure is enough to prevent most if not all of the negative changes we should be concerned about. Adrenergic changes create a more "fit" body.

Everyone should be concerned about cardiac remodeling, whether using AAS or not. That's where supplementation and living healthily come into play. That may sound kind of vague, but there are too many powerful supplements available that directly protect the heart, and we need those anyway, AAS or not.

And here is an interesting paper that discusses some of these issues. I didn't finish it yet but so far, it is worth the read:

Androgen Effects on the Adrenergic System of the Vascular, Airway, and Cardiac Myocytes and Their Relevance in Pathological Processes

Androgen signaling comprises nongenomic and genomic pathways. Nongenomic actions are not related to the binding of the androgen receptor (AR) and occur rapidly. The genomic effects implicate the binding to a cytosolic AR, leading to protein synthesis. ...

www.ncbi.nlm.nih.gov

 

[Jin23]

Well, it's common sense but are adrenergic effects really always a bad thing/contributor to AAS induced negative cardiac remodeling? I'm going to bet that controlling the pressure is enough to prevent most if not all of the negative changes we should be concerned about. Adrenergic changes create a more "fit" body.

Everyone should be concerned about cardiac remodeling, whether using AAS or not. That's where supplementation and living healthily come into play. That may sound kind of vague, but there are too many powerful supplements available that directly protect the heart, and we need those anyway, AAS or not.

And here is an interesting paper that discusses some of these issues. I didn't finish it yet but so far, it is worth the read:

Androgen Effects on the Adrenergic System of the Vascular, Airway, and Cardiac Myocytes and Their Relevance in Pathological Processes

Androgen signaling comprises nongenomic and genomic pathways. Nongenomic actions are not related to the binding of the androgen receptor (AR) and occur rapidly. The genomic effects implicate the binding to a cytosolic AR, leading to protein synthesis. ...

www.ncbi.nlm.nih.gov

I was more intrigued by the potential negative psychological effects that upregulated adrenergic signaling might have. Long term aas use always stood out to me as a good method to induce something akin to a state of chemical induced ptsd - and this specific moa fits this notion quite well.

Regarding heart remodeling, I'm not really interested in entertaining this discourse atm, but that's not to say that it isn't interesting or an important topic.

 

[Type-IIx]

This post deserves a bump.

*Didn't know aas change alpha/beta receptor expression and sensitivity. That's a good catch!

The change in the ionotropic response to adrenergic activity occurs in cardiomyocytes and cannot be extrapolated to other types of cells, if that's what you're suggesting.

 

[Jin23]

The change in the ionotropic response to adrenergic activity occurs in cardiomyocytes and cannot be extrapolated to other types of cells, if that's what you're suggesting.

Yes, that was the general direction of my reasoning. But I haven't done any further reading on it, so it was just a presumption. But in any case, the primary point was to bump up that post as it's really solid and more people should read it and give it some serious thought. While heart remodeling is somewhat a known fact in the aas community, specifically LVH, I don't think that most people realize how significant these changes are and that by far don't just include LVH ...

 

[Type-IIx]

Yes, that was the general direction of my reasoning. But I haven't done any further reading on it, so it was just a presumption. But in any case, the primary point was to bump up that post as it's really solid and more people should read it and give it some serious thought. While heart remodeling is somewhat a known fact in the aas community, specifically LVH, I don't think that most people realize how significant these changes are and that by far don't just include LVH ...

These mechanisms are, at least in part, probably what underlie LVH, diastolic dysfunction, and eventual congestive heart failure, in long-term AAS abuse.

 

[guyfawkes1010]

Luckily I get an echo every year or so to check my aortic bulge. Very small right now. In fact so small they are not sure it's not just a shadow lol. But if I start to see remodeling I would assume it will show up.