Injecting testosterone subcutaneously

[SWALE]

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.

 

[Sunkist]

"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.

 

[SWALE]

Why do you think 6-OXO has a place in this?

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.

 

[frankwhardy]

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_education/pepubs/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

 

[SWALE]

Thank you for your detailed report.

Yes, we'll be interested to read whether you experience the burning sensation again.

 

[LiquidGib]

Your work as making yourself a lab rat is greatly appreciated!

 

[Albert]

I liked Sub-Q............

I think that sub-q injections are the way to.

I did it for several months and found I had a couple of lumps where I had been injecting.

I got worried and started to do IM again, but found they disappeared in a few weeks and went back to sub-q again.

I am now trying Testogel, but thru lack of doctors support, I am thinking of going back to injections as I felt better doing weekly sub-q.

I think I would spend more time on needle lenght and position if I was to start again.

It will suit some people but not others, just as gels suit some and not others.

Later,
Albert.

 

[Sunkist]

Transdermal DHEA

Why do you think 6-OXO has a place in this?

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.

 

[frankwhardy]

Hi Sunkist,

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

 

[SWALE]

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).

OUTSTANDING observation about DHT, E and BPH!

 

[SPE]

Here is an interesting study on transdermal DHEA. From what I can tell, the dose used is something like 142 mg/day!

Physiological changes in dehydroepiandrosterone are not reflected by serum levels of active androgens and estrogens but of their metabolites: intracrinology.

Labrie F, Belanger A, Cusan L, Candas B.

Medical Research Council Group in Molecular Endocrinology, Centre Hospitalier de l'Universite Laval Research Center, Le Centre Hospitalier Universitaire de Quebec, Canada.

This study analyzes in detail the serum concentration of the active androgens and estrogens, as well as a series of free and conjugated forms of their precursors and metabolites, after daily application for 2 weeks of 10 mL 20% dehydroepiandrosterone (DHEA) solution on the skin to avoid first passage through the liver. In men, DHEA administration caused 175%, 90%, 200% and 120% increases in the circulating levels of DHEA and its sulfate (DHEA-S), DHEA-fatty acid esters, and androst-5-ene-3 beta,17 beta-diol, respectively, with a return to basal values 7 days after cessation of the 14-day treatment. Serum androstenedione increased by approximately 80%, whereas serum testosterone and dihydrotestosterone (DHT) remained unchanged. In parallel with the changes in serum DHEA, the concentrations of the conjugated metabolites of DHT, namely androsterone glucuronide, androstane-3 alpha,17 beta-diol-G, and androstane-3 beta,17 beta-diol-G increased by about 75%, 50%, and 75%, respectively, whereas androsterone-sulfate increased 115%. No consistent change was observed in serum estrone (E1) or estradiol (E2) in men receiving DHEA, whereas serum E1-sulfate and E2-sulfate were slightly and inconsistently increased by about 20%, and serum cortisol and aldosterone concentrations were unaffected by DHEA administration. Almost superimposable results were obtained in women for most steroids except testosterone, which was about 50% increased during DHEA treatment. This increase corresponded to about 0.8 nM testosterone, an effect undetectable in men because they already have much higher (approximately 15 nM) basal testosterone levels. In women, the serum levels of the conjugated metabolites of DHT, namely androsterone glucuronide, androstane-3 alpha,17 beta-diol-G, androstane-3 beta,17 beta-diol-G, and androsterone-sulfate were increased by 125%, 140%, 120% and 150%, respectively. The present study demonstrates that the serum concentrations of testosterone, DHT, E1, and E2 are poor indicators of total androgenic and estrogenic activity. However, the esterified metabolites of DHT appear as reliable markers of the total androgen pool, because they directly reflect the intracrine formation of androgens in the tissues possessing the steroidogenic enzymes required to transform the inactive precursors DHEA and DHEA-S into DHT. As well demonstrated in women, who synthesize almost all their androgens from DHEA and DHEA-S, supplementation with physiological amounts of exogeneous DHEA permits the biosynthesis of androgens limited to the appropriate target tissues without leakage of significant amounts of active androgens into the circulation. This local or intracrine biosynthesis and action of androgens eliminates the inappropriate exposure of other tissues to androgens and thus minimizes the risks of undesirable masculinizing or other androgen-related side effects of DHEA.

PMID: 9253308 [PubMed - indexed for MEDLINE]

 

[SWALE]

...I'll be thinking about that one for a while. Great find!

 

[RitchieC]

I found it interesting that the implantable testosterone pellets are implanted Sub-Q.

Anyhow, I tried a sub-Q injection today using a 23G 1" needle. Like one of the previous posters, I noticed a mild burning sensation, nothing too awful.

It was a lot easier than self-injecting IM (I usually have someone else do that for me, but sometimes that just doesn't work out).

 

[Weatherlite]

Yeah it's a lot easier because there are no nerve endings in the lower layers of the skin...only the outer. However, a 23G for sub-q? Is that all you had? I use 31G at 5/16" and it works fine with ZERO pain.

 

[MANWHORE]

31G at 5/16" and it works fine with ZERO pain.

Holy shit,i wouldn't even feel that go in. I use a 28g 5/8"

 

[RitchieC]

it was either a 23g 1" , a 22g 1.5" or a 21g 1.5" or and 18g 1.5" (holy crap!). I didn't think that you could use something as small as 28g.

after reading this again, I tried a small amount using a 29g 1cc slin pin.

I had to heat up the oil to body temperature (just used warm water in a coffee cup and put the vial in there for a while).

After that, it took maybe a minute or two to draw up 0.5cc and about the same to inject it.

it was totally painless.

I am thinking of going this route. I like the ease of injection, and avoiding those annoying "knots" that i sometimes get in my ass for a few days at a time.

And I'm always concerned about the possibility of an abcess (despite sterile injection techniques - which don't seem to be any guarantee against such problems).

Apart from concern (but no proof) of higher e2 levels, are there any other problems with subQ (aside from injecting smaller amounts more frequently)?

 

[cpeil2]

Yeah it's a lot easier because there are no nerve endings in the lower layers of the skin...only the outer. However, a 23G for sub-q? Is that all you had? I use 31G at 5/16" and it works fine with ZERO pain.

But for hCG, yes? I can't imagine injecting Cyp with a 31G.

 

[MANWHORE]

o yeah i'm only talking about HCG,HGH,PGF,IGF,CHG .. stuff like that. I wouldn't even try getting oil into a 31 or even a 27g. I don't even draw up oil in my 23g. I use an 18 and then switch the pins

 

[Weatherlite]

Me either. I just can't see sub-Q with 23G! 27 yes.

 

[frankwhardy]

it was either a 23g 1" , a 22g 1.5" or a 21g 1.5" or and 18g 1.5" (holy crap!). I didn't think that you could use something as small as 28g.

after reading this again, I tried a small amount using a 29g 1cc slin pin.

I had to heat up the oil to body temperature (just used warm water in a coffee cup and put the vial in there for a while).

After that, it took maybe a minute or two to draw up 0.5cc and about the same to inject it.

it was totally painless.

I am thinking of going this route. I like the ease of injection, and avoiding those annoying "knots" that i sometimes get in my ass for a few days at a time.

And I'm always concerned about the possibility of an abcess (despite sterile injection techniques - which don't seem to be any guarantee against such problems).

Apart from concern (but no proof) of higher e2 levels, are there any other problems with subQ (aside from injecting smaller amounts more frequently)?

Hi Ritchie,

How do you find the absorption of the subQ to be compared to IM? For me, the subQ seems a little slower to absorb but more steady/level overall. The avoidance of the "knot" issue that sometimes develops one or two days after an IM injection, and that can last for one or two days, is a benefit of subQ injection in my opinion, too. My only issue with the subQ so far is that, especially for the first day or two, the subQ "lump" that is present seems a little vulnerable to possible injury, e.g., if you've injected into your leg and then are struck there at the site of the injection for some reason (an errant baseball, or whatever), the oil "balloon" that is present (and which is gradually absorbed over several days) might behave similarly to a water balloon, i.e., it might "pop," and possibly create a (non-bacterial) abscess. If instead of 0.5mL (100mg T-cyp) once a week, a person did a smaller volume of 0.25mL twice a week then I don't think even that issue would be present.
Frank