What Are Signs That One's Therapeutic Dose is Too High?

How do you know whether AR stimulation within the myocardium is in the upper bounds of acceptable from TRT

there are many guys who run full on cycles for decades and decades, come out fine… others drop dead after a few cycles

Genetic predisposition and susceptibility play massive roles… furthermore, it’s actually debated whether cardiac injury from AAS stems from AR binding at all, you’ve got induced systemic vascular resistance raising BP (one study found on average the avg AAS user in cycle was significantly hypertensive), beta adrenergic receptor upregulation etc are numerous hypothesised mechanisms

Furthermore data still remains slightly conflicting regarding how severe the effect of AAS on the heart actually is, and these effects appear to be primarily observed with very high dosages 700-1000mg + weekly over prolonged periods of time… I’m not going to defend or condone AAS use as I firmly believe it does lead to cardiovascular disease, especially in those predisposed… but trt or even “optimisation” I think if HCT/RBC/lipids, blood pressure and whatnot are kept in check, you’re far less likely to take 30 years off you’re life than if you’re using very high dosages continuously

There’s another study indicating (new) profound neurotoxicity stemming from human subjects on AAS

All of these studies fail to account for compounds used, not all AAS are the same, there’s a MASSIVE difference between say, primobolan and cheque drops… it’s like comparing cannabis to fentanyl… it’s a stupid comparison to make

To state AR binding inducing a hypertrophic stimuli in cardiac myocytes is the causing mechanism for AAS mediated cardiomyopathy is a very bold and somewhat controversial statement to make… Ive seen the in vitro studies, but what happens on a micro vs microbiological scale differs tremendously, there are numerous bodybuilders who surprisingly have ECG’s/x-rays/EKG’s and whatnot that still check out… in vitro doesn’t account for antioxidant enzymes, elimination pathways etc

We know for a fact that there is a threshold for negative outcomes of AR stimulation. Do we know exactly where it is across all tissues? No. Frankly it’s beside the point. The goal should be to find the best theraputic outcome at the smallest dose. And the holy grail for that is to figure out person to person and tissue to issue AR sensitivity variation.

Whoever finds a way to quickly/cheaply test AR sensitivity to calibrate the optimum dose will become very rich

Though other parameters (bodyfat percentage, lifestyle, age etc) would also need to be considered

Okay, I agree with the points you have made. I think the one thing that you are missing is what happens after the vacuum is pulled.

The reason flow occurs is because there is a difference in pressure. The syringe vial system is trying to reach equilibrium. Meaning trying to get even pressure between the two. So as flow occurs the vacuum in the syringe drops, and the positive pressure in the vial also drops. I don’t see how the last sentence can’t be true, and if that’s the case, wouldn’t in the case of injecting one mL of air and pulling vacuum with 60mL of volume make it more difficult to reach equilibrium vs a 1 mL syringe. Meaning the syringe filling with test has a much larger impact on the filling time with the small syringe than the large.

100%, this is likely one of the huge factors. And it’s within everyone’s grasp now. I’ve noticed as my overall health parameters have improved. So has my response to TRT. I can totally see how the body would react to a more sedentary, poor diet lifestyle by downregulating androgen receptors because it determines it doesn’t need them! Like saying, ‘Well, it doesn’t look like we’ll be doing any fighting or fucking’. The inclusion of Carnitine(2-3g twice per day) has helped me and there is a lot of research out there pointing to how Carnitine mediates AR receptor sensitivity and density. It’s not the kind of thing you’ll see a TRT clinic focusing on tho. Because it’s a path to getting more for less.

I’ve seen the research regarding carnitine and AR sensitivity… I supplement with it too! That and for beneficial effect on lipolysis

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Right so far.

But again, your agrument seems to be built on the idea that the volume that has been evacuated affects the pressure differential. It doesn’t. Again, if we assume low dead space syringers (since they’re the most beneficial to your theory), then as soon as you pull 0.1ml (100 times the dead space) you’re at 99% vacuum. Every additional 0.1ml you pull the plunger adds 2 9s to the percent vacuum…ie .3ml would be 99.9999% vacuum. Not all that much more “pull” than 99%.

Let’s look at this another way…Airliners are pressurized to ~ 8,000 feet equivalent, or somewhere in the neighborhood of 10 psi atmospheric pressure. When they fly at 36,000 feet, the external pressure is more like 3 psi, meaning there’s a 7 psi difference. The door on a 767 is about 74x42 inches…or 3100 square inches and change. That means to pull the door open at 36000 feet, you’d need to pull on the door with approximately 7 * 3100 = 21,700 pounds of force. The size of the airplane doesn’t matter. The size of the door does. And bringing this back to our example, it is the diameter of the needle that affects fill rate, not the size of the syringe.

On the flip side, when you’re doing your injection, you’re limited by your own strength and the integrity of the syringe - instead of being limited to pulling ~ 14 psi of vacuum you could in theory put dozens of pounds of push on the plunger which will help your flow rate.

Where can you find a trustful information about the real side effects of certain SARMs? I guess they fuck the lipids as well?
Is there are a SARM that seems safe if you are on TRT?

Or simply reduce the dose by a lot, in my case 0.25 mg of arimidex made feel terrible, i had to microdose it, dissolving 1 mg pill in vodka and taking far less of a dose as low as 0.05 mg

@vonko1988
But why? They aren’t safer than doing more Test and they give half the results at best. We have a lot of literature on steroids and there’s a whole section here full of people using them effectively. Most of the guys using SARMs are either scared of needles, stupid enough to believe they don’t “shut down natural test”, or think because they don’t pack on as much muscle that they are safer. Just do steroids. People have been using them for almost 100 years. You can triple your test dose and get pretty fucking big in 12 weeks relatively safely or you can take some SARMs gain half the muscle and pray you a) actually got what your think you bought b) roll the dice on what effects it has on you short & long term. If you’re going to do it (and really you shouldn’t until you’ve been on TRT for a year and have a decent base w/ diet in check at the minimum) do 500mg of Test for 12 weeks and be a grown ass man. You should be able to gain quite a bit on TRT especially the first year or two. I haven’t gotten to the point where I feel the need to go full steroid cycle as I continually get gains from TRT. Eventually I likely will though but until then…

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They most certainly do…

Is there a synthetic androgen that seems safe if you’re on TRT?

It’s literally the same question, they probably aren’t much safer than gear… but with less benefit (regarding added muscle mass)… we need data regarding how they affect one neurologically in high dosages

I understand. Thought similar but still I have no idea of SARMs so had to ask.
If I do something more it will be at least after a year. Ive also considered 300-500mg of test but will need to take care of the really high e2 I will get and I do not wanna mess with AI, hope proviron can do the job to stop the symptoms

This is a bit off. My argument is that while a syringe fills the pressure differential between the syringe and vial goes down, and the characteristics of the drop in pressure differential will be impacted by the size of the syringe.

I understand that initially we have about 1 atm of difference in both cases. I do not buy that the when .5 mL is filled in both a 1 mL and 60 mL syringes that are fully pulled back that both syringe vial systems have the same pressure differential. I believe the 60 mL syringe vial system will have closer to 1 atm difference between the syringe and vial and that the smaller 1 mL syringe will be about half the pressure difference.

No arguments about the amount of vacuum at the start. It is the same. I believe that if we were to plot Delta_P for both systems (1 mL and 60 mL syringe and vial) that the 1 mL drops much faster and reaches very close to 0 when full. The 60 mL I would think would drop slower and not get close to 0 in the case that we pulled the plunger all the way back, and only filled 1 mL or 1/60th of the syringe volume.

Dude forget about Sarms. You are just getting going with TRT. You finally found a protocol that seems to be working for you. Enjoy it for a year. If you want more for asthetic reasons or just plain curiosity add in a little Mast P, NPP , blast down the road.

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@mnben87

Not sure what to tell you man. I can and have given you examples to try to explain the concept based on known scientific principles rather than “what you think”. There’s a grain of truth in your belief but it is limited to use of normal / high dead space syringes. With a high (80-100 ul or more) dead space, you need to overdraw the syringe by by 8-10 ml, perhaps more, in order to achieve the level of vacuum you get in an insulin syringe with only 0.1ml overdraw…so clearly/obviously the larger syringe is a benefit when using standard needles. The limit is the degree (percentage) of vacuum you can achieve and the diameter of the needle.

The problem is that you haven’t addressed my issue with the concept of Delta_P decreasing as the syringe fills. You keep going back to dead space syringes. I get that they both create the same vacuum at the event of drawing back the plunger.

This is not me going with “what I think”. I am using sound logic and principles of physics. I will accept not being correct if you sufficiently explain why Delta_P (the driving force of fluid flow) will not drop faster with a smaller syringe as compared to a larger syringe.

I mean the reason we have flow is because the pressure difference (Delta_P) between the syringe and the vial is trying to even out. Now that pressure difference evens out as the syringe fills, right? Now that filling effect is much smaller if you are using a huge volume vacuum than a small one, right? This is what I want want explained. If you do that I’ll agree you are correct.

The pressure differential is between the interior of the vial and the interior of the syringe. I will discuss this in terms of PSI but if you have a preferred unit of pressure we can convert easily enough.

Can we agree that the vial’s contribution to the pressure differential is irrelevant? Clearly the syringe choice is not going to change whatever pressure/vacuum level is in the vial.

We will also ignore the idea of dead space since you don’t like that either. So we have a syringe with an ideal needle that have absolutely nothing in them - the “dead space” is zero. With zero dead space, the instant we pull the syringe back .00001 ml, that creates an instant, absolute, 100% vacuum. Relative to the atmosphere that would be somewhere around 14.7psi as I’ve said. Whatever it is relative to the vial is what it is. Volume does not factor into vacuum. You cannot create additional “vacuum effect” by enlarging the evacuated space. That is the scientific principle - pressure differential is not dependant on the volume of the pressurized (or evacuuated) space.

synthetic androgens that aromatise less and/or don’t aromatise exist… short term, primo is likely safer than test mg/mg (aside from dyslipidemia induced)

I am okay with this.

Agree here.

Agree.

Agree, but what happens to the vacuum when the syringe fills? When the syringe is almost full does it still have a difference of 14.7 PSI relative to the vial? Putting matter into a vessel that is holding vacuum increases the density of vessel’s holdings and increases pressure. I am arguing that since the density change in the small syringe is much more significant, that there is a much larger impact on Delta_P. As Delta_P drops so does fluid flow as Delta_P is what is driving fluid flow. Does this makes sense?

This makes sense to me, but it is possible I am missing something. I am not saying you are wrong, just that I am not convinced you are right just yet.

As T starts flowing into the syringe, the syringe will then contain T and vacuum. Because there will still be some portion of total vacuum (volume to which the plunger has been drawn minus the volume of T that has flowed), the exact same level of total level of vacuum will continue to exist. From the syringe’s “point of view” as long as there’s even .001 ml of “total vacuum” in the syringe, it’s pulling as hard as it possibly can.

From the vial’s point of view, because the T vial is shipped with some “air space” it is at some level of pressure (probably close to 14.7 psi - let’s assume that for convenience) relative to the syringe at the start. As the T is sucked into the vacuum of the syringe, the level in the vial drops. If, for example, you start with a vial that has exactly 1ml of your Mannzoil and .25ml of air, then after you pull .25ml of T, the head space has doubled and therefore the pressure differential has dropped in half (say 7.35 psi). Keep pulling another .25 ml and your pressure is now down to (14.7/3). You cannot increase the pressure differential by pulling harder on the syringe.

What would work? Yank the plunger out of an insulin syringe and stick it into the vial in addition to the syringe you’re drawing with. :wink: Then you’re never inducing low pressure in the vial and the juice will flow at a constant rate.