Established truths and controversial claims

[hammerheart]

My T is at the low range of normal. Has been ever before I started AAS. That is why I decided to go on. I always seemed to have trouble recovering from workouts, low energy, mental fog and all that. I was to young when it was discovered and no MD would put me on TRT. Even though I had both symptoms and confirmtive tests to back up their diagnosis to anyone. Finally I decided to try it and loved it, loved how I finally felt normal and loved how I could finally lift without some silly injury popping up over time.

Those where my very symptoms for the whole of my life, and my T scored 159 ng/dl at 24. "Luckily", I had no problem getting prescribed TRT, but thing got only worse since.

Was really thinking of going HCG only as a base for TRT then stack 19-nors atop that, but this means long-term (largely unknown) implications.

Or I can just use HCG and a bit of test in order to get ratios straight, ie enough E2 at physiological levels of T.

Can't you use your knowledge to help me sort this out? A knowledge check? Firstly I understand the issue to be completely in the CNS. Given how fast the symptoms develop, my suspect go to neurosteroids able to induce rapid changes in neuromodulation - either fluctuation in E2 or DHT derived -diols, which are potent GABA-A allosteric agonist. It's like my brain can't adapt to these how it should, hence the symptoms, which sounds like serious anxiety issues but if I were THAT anxious then I guess I would be panicking, and my BP through the roof, where it's normal. In fact, I used to experience both hypotension and bradycardia (40-45bpm). When I did gels this was so strong I was unable to move. Eventually, after correcting hypothyroidism, this subsided. It much sounds like and imbalance between inhibitory and excitatory factors... I've experimented with many compounds and the only ones able to reverse symptoms are those that concomitantly enhance both DA and NE.

Does this reasoning makes any sense to you?

[Bio-Active]

If that's the problem then why doesn't tren worse it all? Isn't it regarded as much stronger than Test?

Btw I want to lower it and that's why I'm using winstrol to dial down SHBG.

Just because its stronger then test doesn't mean much as we all react different and tren sides are nothing like test sides.

[DocToxin8]

But Tren doesn't convert by 5AlphaR, so it is stronger really?
(Except in muscle tissue ofcourse)

As for your symptoms Biz, how do you know it's sex steroids which cause them?
While it definitely sounds like you need TRT, and will suffer possible sides from that, something else might also be going on.

If you think it has to do with gabaergic overactivity, then see if your doc could prescribe flumazenil to try that out. (Might be hard though)
Or, more likely I would think, it might be the endorphin system, in which case you could try low level naltrexone treatment. Something that has helped a lot of cases, not only those related to endogenous opioid dysregulation.

And how do DA agonists/releasers like dextro-amph. work on you?

[hammerheart]

But Tren doesn't convert by 5AlphaR, so it is stronger really?
(Except in muscle tissue ofcourse)

As for your symptoms Biz, how do you know it's sex steroids which cause them?
While it definitely sounds like you need TRT, and will suffer possible sides from that, something else might also be going on.

If you think it has to do with gabaergic overactivity, then see if your doc could prescribe flumazenil to try that out. (Might be hard though)
Or, more likely I would think, it might be the endorphin system, in which case you could try low level naltrexone treatment. Something that has helped a lot of cases, not only those related to endogenous opioid dysregulation.

It's indeed an issue in the GABA! However you should also know the GABA receptor respond in a U-shape fashion - ie. after a certain saturation point is reached "paradoxical" reactions kick in.

No idea about the opioid system, I don't know it well, but having an autoimmune disease might be playing a role there.

I know the Test triggers it, however I do realize the issue is with my brain and not the sex hormones themselves, but I must find a balance, it's not that I have to stack this or that in order to get things to work.

And how do DA agonists/releasers like dextro-amph. work on you?

Best, they make me feel normal like I haven't in a long time.

[hammerheart]

But Tren doesn't convert by 5AlphaR, so it is stronger really?
(Except in muscle tissue ofcourse)

It should be as strong as DHT to my understanding, but even on low dose you are going to reach concentrations way above DHT ones, and Tren doesn't even bind to SHBG like DHT.

Just because its stronger then test doesn't mean much as we all react different and tren sides are nothing like test sides.

Of course I know that, but it activates the AR in the same way as Test, what I'm trying to do here is to sort our which component is triggering the symptoms.

[Bio-Active]

Bizz are you seeing an endo?

[hammerheart]

Not anymore, he wasn't really of any help, even if he's a researcher and professor at the local university.

[Bio-Active]

Not anymore, he wasn't really of any help, even if he's a researcher and professor at the local university.

gotcha it's important to have someone you are comfortable. I didn't like my first one so I had him refer me to a different one then after we got things sorted out I just switched to my primary care.

[MuscleScience]

Not anymore, he wasn't really of any help, even if he's a researcher and professor at the local university.

Have they checked your gonadotropin levels. To me from what you have said. You have more of a central endocrine disorder vs it being a gonadal issue or receptor mediate me issue.

[MuscleScience]

Or I should say your gonadal tropic releasing Hormone levels?

[hammerheart]

Or I should say your gonadal tropic releasing Hormone levels?

Diagnosis is hypogonadotropic hypogonadism, so yes the issue is hypothalamic in origin, not gonadal.

[MuscleScience]

(I'm sorry but I'm very busy today, will contribute more tomorrow, glad to see the thread going.)
There's always some "established truths" about everything from training to diet to AAS. Like, use test as base, use an AI, do PCT with nolva and clomid but not hCG, which should be run during cycle, etc.

Dont do oral only cycles, etc.
I will jump back in tomorrow guys!

I sometimes do oral only cycles. All these drugs were designed to be stand alones. There is virtually no primary evidence that I have been able to find or that someone has shown me that actually talks about stacking. The only thing with sex hormones and multiple types together is in the birth control Or infertility literature. Secondly almost all athletic or sports doping cases to this point have been busted with only one anabolic compound and sometimes ancillaries.

A lot of the state sponsored programs before testing only had athletes on one compound. T-bol of course being the prime example.

Lastly, does the body really see synthetic T as the same as endogenous T? If so, there is no reason that spermatogensis should be shut down if the body viewed it as the same and it wasn't out of physiological range. Thus does having synthetic T really help you during a cycle to keep low T symptoms at bay?

To me, from what I have read. Shut down is shut down no matter the compound. So why dilute the effectiveness of a compound by introducing another compound that is competitive in nature for the same receptor spots. This is exactly the principle as to why SERMs were designed.

Again, these are all the questions I have in my mind when I think about a cycle design.

[MuscleScience]

Questions I have without having seen satisfactory evidence for the answers that is.

[DocToxin8]

I sometimes do oral only cycles. All these drugs were designed to be stand alones. There is virtually no primary evidence that I have been able to find or that someone has shown me that actually talks about stacking. The only thing with sex hormones and multiple types together is in the birth control Or infertility literature. Secondly almost all athletic or sports doping cases to this point have been busted with only one anabolic compound and sometimes ancillaries.

A lot of the state sponsored programs before testing only had athletes on one compound. T-bol of course being the prime example.

Lastly, does the body really see synthetic T as the same as endogenous T? If so, there is no reason that spermatogensis should be shut down if the body viewed it as the same and it wasn't out of physiological range. Thus does having synthetic T really help you during a cycle to keep low T symptoms at bay?

To me, from what I have read. Shut down is shut down no matter the compound. So why dilute the effectiveness of a compound by introducing another compound that is competitive in nature for the same receptor spots. This is exactly the principle as to why SERMs were designed.

Again, these are all the questions I have in my mind when I think about a cycle design.

Stacking hasn't been studied well no, but it makes sense. AR binding isn't the whole story or anadrol would be useless. Also AR aren't like Alpha1 adrenergic receptors, they don't down regulate when stimulated, I actually think they upregulate.
Also imagine you stack T with DBOL,
DBOL should have greater impact on liver IGF1 secretion than T. But it has lesser affinity for the AR.

T would also ensure physiological functions like libido by converting to DHT in brain and testes.

Synthetic T is exactly the same as endogenous T. Once Test e enters the blood stream the ester is rapidly removed by esterases, and the remaining T identical to your own.

These agents were developed first, then put into use were they could find use for them. Pretty much like most drugs. Viagra was never intended for ED, but proved ineffective as a BP lowering agent in heart patients. But heart patients often have ED and didn't want to stop using Viagra, and they (drug company) realized they failed and struck gold at the same time.

Many AAS were developed as attempts to replace T, but couldn't really do that. But they soon found out it they could have other benefits.

Small doses of DBOL could be used as a tonic, as it wouldn't supress you 100% right away with small doses.

[DocToxin8]

And spermatogenesis stops because LH and FSH signaling stops, because there a feed back loop for sex hormones. When they're high the brain (hypo and pit) notice and stops sending FSH and LH to the testes.

If you use HMG while on cycle spermatogenesis wouldn't stop.

In theory if you used several grams of test a week spermatogenesis shouldn't stop either for a long time, since T alone seem to be enough.
But the testicles have about 100x higher T concentration than the rest of your body. So even when you use 750mg a week the testicles are "starved" for T.

[InternalFire]

after reading this I just want to pump this to the top