Men's Health Forum: This is a discussion on Injecting testosterone subcutaneously within the Anabolic Steroids forums, part of the extensive steroid information at MESO-Rx; Negative. Directly exposing T to aromatase elevates E's. I do not know by how much, but SC injections would have ...
Negative. Directly exposing T to aromatase elevates E's. I do not know by how much, but SC injections would have to raise E more than IM.
And we do not want to use additional medications where unnecessary.
I would like to see evidence that SC produces more stable androgen levels than IM does. While this does happen with HCG, it is not an analogous situation.
"Fat tissue: a steroid reservoir and site of steroid metabolism
JP Deslypere, L Verdonck and A Vermeulen
Sex steroid concentrations and 17 beta-hydroxy-steroid dehydrogenase and aromatase activities were determined in fat tissue removed at surgery or, in order to allow comparisons in different sites, postmortem. Except for dehydroepiandrosterone (DHEA) sulfate (DHEAS), there existed a positive tissue/plasma gradient for all steroids studied (testosterone, androstenedione, DHEA, androstenediol, estrone, and estradiol), suggesting androgen uptake and estrogen synthesis in situ. Androgen concentrations did not vary according to site of origin of fat tissue, except that the DHEAS concentration was significantly lower in abdominal sc and omental fat than in breast, pericardial, or sc pubic fat. Tissue androgen concentrations were positively correlated with their plasma concentrations, but tissue and plasma estrogen concentrations were not correlated. All tissue steroid concentrations, with the exception of estradiol in men, decreased with age. Aromatase activity [androstenedione----estrone; mean maximum velocity, 7.4 +/- 3.7 (+/- SD) fmol estrone/mg protein . h] did not vary between sexes or with site of origin of fat tissue. 17 beta-Hydroxysteroid dehydrogenase activity (estradiol----estrone, mean maximum velocity 9.8 +/- 5.4 pmol/mg protein . h) was higher in fat from women than in that from men, higher in premenopausal than in postmenopausal women, and higher in omental than in sc fat. Its activity was noncompetitively inhibited in vitro by DHEA and DHEAS in near-physiological concentrations, and the enzyme activity was inversely correlated (P less than 0.001) with the tissue DHEA and DHEAS concentrations. We conclude that fat tissue is an important steroid hormone reservoir, that it is the site of active aromatase and 17 beta-hydroxysteroid dehydrogenase, and that tissue DHEA(S) may have a modulating effect on tissue estrogen production. "
There is some really good stuff ( vivo and vitro) out there right now about transdermal DHEA, which should be an adjuct to any TRT. Also it seems the estrogen is retained to a greater degree in fat while the T is released into the blood. Lastly the site of the fat seems important, and I wonder if degree of vascularity has input here. With all the potential for problems, I would still go subq if I were going to go needle. One is going to aromitize anyway with elevated T levels, so ascorbic acid and 6-oxo are part of the arsenal.
I hqave no experience in using it this way, but have seen a couple of pieces which claimed transdermal DHEA did not convert into estrogen, if memory serves.
What gauge and length needles do you use for this?
This Forum has a very good relationship with H2, as well as the Fina Group. We encourage all of our members to participate wherever they may receive benefit.
Frank, from a commercial standpoint, using your logic, from a commercial standpoint, wouldn't it make more sense for them to want to sell as much as possible?
But you are correct in that I am ocncerend about injecting oil into fat. And aromatase does live there.
Maybe they are onto something, I just don't know. But it just does not seem prudent to me at this itme. Maybe someday I will change my mind.
Hi Dr. C,
Regarding the commercial standpoint, my thinking was that if the Depo-T or similar product can be marketed to the hypogonadal/HRT patient as an injection that need be given only once or twice a month versus once or twice a week then there might be a greater acceptance and hence better sales, since a lot of people are needle-adverse and it makes for fewer trips to the doctor's office (for those that don't want to self-inject).
I went ahead an initiated an experiment myself earlier today with my weekly T-cyp injection of 100mg (200mg/mL concentration). Using a 28 guage, 1/2" insulin syringe, I injected 0.5mL subQ at a 90-degree angle into pinched skin over the vastus lateralis. (I followed the guidelines regarding location and technique found here: http://www.cc.nih.gov/ccc/patient_ed...epubs/subq.pdf) The injection went very well with no blood or oozing of oil. Drawing the very viscous testosterone cottenseed oil took 3-4 minutes with the tiny gauge needle, but was not a problem. The injection did not leave a visible bump under the skin (although if I used my imagination I could possible see one), but one can feel a slightly raised area. Within seconds after the initially painless injection there began a very mild burning sensation, not present with intramuscular injections I've done, which persisted intermittently over nearly 2 hours, gradually diminishing. The burning sensation was similar to, but less than what one might experience with rubbing alcohol going into a tiny paper cut, and was mostly produced by movement/stetching of the skin with physical activity. I have no idea if the burning is due to the testosterone ester, the cottonseed oil, or the benzyl alcohol preservative (just guessing, probably the alcohol?).
I'll report back on my subjective experience regarding how the subQ injection compares to IM with regard to onset, duration and quality of action of the T (as best I can - it's been about 12 hours or so now since the injection and I really can't tell much difference between the subQ and the IM injections I've done previously at this point), but right now I'd say that IM is better, so far, simply because of the slight burning sensation that is apparently present with subQ - at least for me in my thigh area, anyway (it is essentially negligible, though, as was mentioned in the quoted earlier post I made). Having the reservoir of T-containing cottonseed oil so close the outer skin layer makes me feel a little "exposed" as well - I'm not sure what would happen if there were some kind of trauma to the area . . .
Frank
Last edited by frankwhardy; 10-03-2005 at 05:52 AM.
I hqave no experience in using it this way, but have seen a couple of pieces which claimed transdermal DHEA did not convert into estrogen, if memory serves.
Unfortunately it is my understanding that DHEA can increase Estrogen levels, by natural transformation, unless one goes directly to DHT, which transdermally some of it does ( to a greater extent in the skin???). The skin is an amazing organ, we just need to use it as such. Transdermal DHEA shows something like a 25-30% ad/absorption rate. Oral is zip.
I read a couple of very interesting studies that attribute transdermal DHEA in quantities far above what I use with transdermal T ( as a combination, I have found stability and kept innate production of Testosterone to a maximum with transdermals of T, Andro and DHEA simultaneously and overlapping as to time frame) ( I have 3 years of blood draws now to go on, and am an advocate of transdermal delivery if for no other reason that it is natural and mimics the body's own release) anyway... the transdermal DHEA seems to cause almost a second puberty at very high levels in middle aged men. I am afraid to go to these levels as they are 20x the body's natural production, but the purpose was anti-aging mostly. Have you seen these? People get tired or reading studies so I won't post any, but I wish I had downloaded them. Very interesting. The search criteria were on DHEA and transdermal.
I like 6-oxo and the look alikes. They seem to, with transdermal chrysin, zinc, and C, to do a decent job of non med anti aromitization. I have not had to go to the med AI yet to keep my E2 in check with a maintained TT at 1000. I am only anecdotal here on the 6's, plus going on web site promos that pass for studies and my own experience: I am aware not valid. I want DHT production BTW. While everything else aromatizes, it doesn't and it prevents BPH as long as the E is kept down, and supports what I want from TRT... wish I had an answer for the hair. Thus the site of the transdermal is very important.
Too bad the government will soon take DHEA away too and make it an RX.
So are you using transdermal chrysin yourself? If so, how much are you using, and is it compounded into your T, Andro and DHEA mixture, or is it a separate preparation? Also, if you started using the chrysin after you began TRT (as opposed to throwing in the chrysin at the start of TRT), do you by any chance have any labs showing what your E2 levels were before and after using the chrysin? I'm just hoping to get an idea of how effective it is. Thanks,
Frank
Sun--I don;t know who you are, as you are new to the Forum, but am impressed with the common sense approach you have achieved. I'm sure we will all enjoy your participation here. We've got some very good Bro's in our little community.
True enough, there are two major drawbacks to oral DHEA supplementation
(1) poor bioavailability and (2) biotransformation into estrogens. The first must be taken into account when drawing labs to evaluate effectiveness of therapy. For instance, most of what appears in urine assay will be from first pass effect, so will falsely--and greatly--elevate the number.
Supplementing 20X normal production to achieve upper range physiological range neither impresses nor scares me. It's the PK's, that's all. We just have to watch for deleterious side effects.
As time goes on, I am gettng more and more interested--nay, fascinated--with transdermals. However, the concept of them producing a more "natural" distribution is, IMPO, overblown.
If the politicians were to actually learn one simple fact about DHEA, namely, that it cannot convert into testosterone in males, they would not be so quick to try to outlaw it. Or not; there's votes out there to grab!
Of note, here we like reading abstracts of interesting studies, and then discussing them. We're kind of sick that way.
I am not in favor of 6-OXO, as, from what I have seen, it favors conversion to estrones (which are already favored to start with).
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