How i finally found a way to go subQ and why i wished....

[JimGainz]

Hello fellas, i have opened a thread a couple months ago where I wrote how Everytime I try to go subQ TRT after 2-3 weeks it's like i am off TRT...
I have tried this 3! Times and always ended up going intra muscular again.
I didn't have any problems with IM injections. But I wanted to inject 3 times a week and didn't want to inject IM that often.
Here is how i solved my Problem. OK! First of all. SubQ works! It really works. If it works for me it will for you too!

I had a bottle of dbols which i didn't use for many years. When I started my 4. Experiment with subQ i took 1 dbol daily for 4 weeks and injected with the insulin small 8 mm needle. Right VG Monday/
Right shoulder Wednesday and left VG Friday.
90 mg total testosterone. Every injecton 30 mg.

Last Week I stopped taking dbol and today i made bloodwork.
Total test: 1000 Ng/dl
Free test: 35 Ng/dl
Estradiol 65.
Wow!
If I stay on this dose I need to take a bit AI here and there. I get symptoms on that number. But overall i feel ok. But since m shbg is 12-18 my androgen index is still through the roof.

I will probably inject 75 mg from now on and call it a day finally. Honestly i think that even 60 mg weekly total puts my total to 600s which is great.

I just write this because I know there are many guys who wanted to try subQ but stopped after 2-3 weeks because the were not patient enough like me. But it seems like when You go subQ from IM on some people or maybe most it needs to build up like you start TRT again. You really need to give it time. And You don't need dbols like me. The only reason I took it was because i just wanted to be sure.
Hope this helps. Sorry for my bad English.

I like the idea of using a low-dose anabolics to kickstart things, whether it’s switching protocols or simply to help with the Recomp. My personal choice would be ianavar. But I’m curious how much Dbol did you use? And did you get liver values tested assess sides?

 

[bennygoestrt]

I like the idea of using a low-dose anabolics to kickstart things, whether it’s switching protocols or simply to help with the Recomp. My personal choice would be ianavar. But I’m curious how much Dbol did you use? And did you get liver values tested assess sides?

10 mg dbol and 20 mg on training days. Didn’t check liver but at that tiny dose which was designed to be trt back then in the 70s there are no health risks if you kickstart them for like 8-10 weeks I would say

 

[madman]

10 mg dbol and 20 mg on training days. Didn’t check liver but at that tiny dose which was designed to be trt back then in the 70s there are no health risks if you kickstart them for like 8-10 weeks I would say

Methandrostenolone was never developed let alone used for TRT.

First compounds on the market (mid-late 1930s) to treat men for hypogonadism were pellets, methyltestosterone, and testosterone propionate.

These were the mainstay for decades until testosterone cypionate and enanthate came on the scene in the 1950s and dominante the market to this day!

Methyltestosterone was dropped from the market ages ago due to the high potential for liver toxicity as it is a c-17 alpha-alkylated oral just like methandrostenolone (Dianabol).

Methandrostenolone (Dianabol) let alone any of the other synthetic AAS would never be used as a sole replacement for testostreone therapy.

Methandrostenolone plays not part in TRT/HRT!




The principal goal of androgen (testosterone) replacement therapy is to restore a physiologic pattern of net tissue androgen exposure in androgen deficient men whose damaged reproductive systems are unable to secrete adequate testosterone to levels comparable with those of eugonadal men. This treatment uses only the natural androgen, testosterone, aimed at restoring a physiologic pattern of androgen exposure using a dose limited to that which maintains blood testosterone levels within the eugonadal range. Such treatment aims to restore the full spectrum of androgen effects when endogenous testosterone production fails due to pathological disorders of the reproductive system (testicular-hypothalamic-pituitary axis). This requires restricting replacement therapy to the major natural androgen, testosterone, which aims to not only replicate physiological circulating testosterone levels but also to provide testosterone’s two bioactive metabolites, DHT and estradiol, so that all 3 bioactive sex steroids are available to androgen target tissues. Synthetic androgens are unsuitable because they are incapable of metabolism to the more potent 5α reduced metabolites or being aromatized to estrogens. The overall goal of such replacement therapy is to replicate the efficacy and safety experience of eugonadal men of similar age by recreating the full spectrum of endogenous natural androgen effects on tissues so as to recapitulate the natural history of efficacy and safety of endogenous testosterone.

Practical Goals of Androgen Replacement Therapy​

The goal of androgen replacement therapy is to replicate the physiologic actions of endogenous testosterone, usually for the remainder of life as the pathological basis of hypogonadism is usually irreversible disorders of the hypothalamus, pituitary or testis. This requires rectifying the deficit and maintaining androgenic/anabolic effects on bone (153, 569), muscle (349), blood-forming marrow (352, 570), sexual function (71, 571), and other androgen-responsive tissues. The ideal product for long-term androgen replacement therapy should be a safe, effective, convenient, and inexpensive form of testosterone with long-acting depot properties providing steady-state blood testosterone levels due to reproducible, zero-order release kinetics. Androgen replacement therapy usually employs testosterone rather than synthetic androgens for reasons of safety and ease of monitoring. The aim is to maintain physiologic testosterone levels and resulting tissue androgen effects. Synthetic steroidal and non-steroidal androgens are likely to lack the full spectrum of testosterone tissue effects due to local amplification by 5α reductase to DHT and/or diversification to act on ERα by aromatization to estradiol. The practical goal of androgen replacement therapy is therefore to maintain stable, physiologic testosterone levels for prolonged periods using convenient depot testosterone formulations that facilitate compliance and avoid either supranormal or excessive fluctuation of androgen levels.