I just have a quick question for any of you out there that are on a doctors prescribed TRT. How much do you inject? How often do you inject? and what type of test do you inject. The reason I’m asking is instead of going off and on a cycle of test I’m just thinking about putting myself on my own TRT for the rest of my life.
I love the way I feel when I’m on test and people in other countries are “on” all of the time, Dr. prescribed or not. Granted I’m not looking for that bulking dose just the right amount to function at a high level all of the time.
[quote]Dynamo Hum wrote:
I believe a good combo would be:
100mg test/w (preferably enan or cyp - split 2x/w)
250 iu hCG EOD
1 mg Adex/w (split into EOD doses)
or low dose letro.
Check out KSman in over35 lifter forum.[/quote]
i personally believe that 100mg wk is gonna be pretty low, unless you are combining that with a serm to “minimize” suppression of natural T …every body responds a little differently but me personally at that dose i felt like …shit my levels come back at around 57 ng/dl at similar dose
to say you are going to manually/self-prescribe trt is a big commitment and probably a bad idea!
so if you are going to make that commitment now, a easier one would be to have blood work done and that would also be a more responsible decision to base your plan on
I’ve been on 100mg/w for my 4 stasis weeks and then 1 wk of 80mg (tapering). My libido is better than it was at 250mg E3D. I am using about 1mg Adex/w currently and no hCG since my cycle ended to facilitate restoring HPTA.
Many in the “Over 35 Lifter” forum do as I recommended with good results. Adding cabergoline to the mix can add to an already good protocol.
Any effective TRT dose will shut down the HPTA. TRT is forever and SERMs are not considered safe for life long use… for several reasons. hCG is the only way to go. That been said, I am finding than an short cycle of a SERM may be of benefit when otherwise in a state if TRT induced perpetual HPTA shutdown; turning on the LH/FSH production in the pituitary. It is known that some releasing hormones in the pituitary have spill over effects on other targets in the pituitary and that that would be part of natural functioning as well.
The flip side is that TRT induced HPTA shutdown can be expected to have some effects on pituitary release of things other than LH/FSH. So that is not really anything well defined, but it is a fuzzy fact that cannot be ignored either. I found that toremifene had some ‘tonic’ value after 2.5 years of HPTA shutdown while on T+AI+hCG. This seems to be a shorter duration benefit, in part probably from increased E2 to which I am highly sensitive and always as one becomes accustomed to any new effect.
Systems in the body are naturally always in a change of balance, nothing stays the same. Something like a short SERM cycle may ‘wake up’ the HPTA repressed pituitary and improve things outside of LH/FSH mechanics. When one is young/normal, the hypothalimus is hitting the pituitary with GNRH pulses -
all of the time. I think that the effect of HPTA shutdown may be more profound than stopping LH/FST release. There is a missing pulse.
Note that a constant level of GNRH can stop LH/FSH release.
I think that the problem is that the receptors get saturated and with the loss of effective pulsatile stimulation, things fail. This is another example of where things do not work right when signals become constant. This raises other concerns about GH releasing hormone and analogs.
GNRH analogs can be used to shutdown the HPTA as a chemical castration. Too much GNRH can have the same effect as none at all. Some things need to be in a state of change and not steady state. Turning off one pulsatile stimulus of the pituitary can be expected to have some unexpected effects as from the spill over into other pituitary functions. Negative effect of this type are probably subtle and slow to take hold. This is TRT territory and may not have any concerns for gear cycles. When someone on TRT for a long time gets a positive effect from a short term SERM cycle, things may then become apparent. The only thing wrong with using a SERM in this situation, is that when it restores GNRH release, that may not be properly pulsatile… something that I do not know about.
KSman - Lets say that someone in a similar situation as you hormonally did use a short cycle of a SERM to try to get the benefits that may be available - If they did in fact stimulate a release of GNRH that was not pulsatile, then what negative things could occur. i mean a steady state GNRH secretion will cause HPTA suppression - but for those on TRT how is this a problem?
Is it not that it would be negative per se, but that the potential positives would not be able to occur (the stimulation and secretion of other related hormones as you suggested)?
Also, you mentioned that when you tried it yourself - the torm - you did notice a positive effect (thats how ‘tonic value’ read to me at least).
Do you think that could have been the initial restart of the HPTA, allowing a small release of neurochemicals and hormones like gonadotrophin-releasing hormone which you noticed before the HPTA was shut down again from the steady state of GNRH?
This is very much guess work from me which is led by you, but i love the subject.
Is there a correlation with this theory and the recovery of the HPTA post gear cycle? i mean, if a prolonged dose of SERM can cause too steady levels of GNRH which will be counter productive - is it possible that EOD dosing for SERM’s during PCT could be warranted?
Certainly, I can get a little depressed, lethargic and slightly irritable on cycle (depending partly on the compounds used). However, this time I have been supplementing with DHEA and have to say I feel much better all round.
That is where hCG is helpful as it also maintains pregnenolone production. AND ONLY 250iu EOD is needed.