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; not sure i can comment on absorption (i assume you're referring to T absorption and not oil absorption)
I'm not ...
I found it interesting that the implantable testosterone pellets are implanted Sub-Q.
This is interesting. I was not aware that the pellets were SubQ. One of the main reasons for using pellets is for more even release of T as well as much less aromatization. If the pellets are SubQ, one would think it would cause more aromatisation. If less aromatization occurs from SubQ pellets, then what would be the difference if one injected T SubQ.
Does anyone have anymore information or thoughts about this?
I found it interesting that the implantable testosterone pellets are implanted Sub-Q.
This is interesting. I was not aware that the pellets were SubQ. One of the main reasons for using pellets is for more even release of T as well as much less aromatization. If the pellets are SubQ, one would think it would cause more aromatisation. If less aromatization occurs from SubQ pellets, then what would be the difference if one injected T SubQ.
One of Dr. Shippen's patients per an earlier post is instructed to do T Cyp SubQ E3D and claims the benefits are more even release as well as LESS aromatization.
Does anyone have anymore information or thoughts about this?
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]
Very interesting study. I had bookmarked it and meant to reply earlier, but had gotten sidetracked.
An interesting question comes to mind. Previous studies - one of which was previously posted on this site - has shown that oral doses of DHEA in higher amounts (the study used 50 mg and 100 mg doses) led to the elevation of estradiol levels in the male test subjects. I note that this test - which uses a transdermal form of DHEA - the test results indicated the following:
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
So the question is.... would a transdermal form of DHEA supplementation be more appropriate than the oral form for individuals known to be low in levels of DHEA/DHEA-S? Is it possible that it is the oral form of DHEA is more likely to convert to / otherwise elevate E2?
I am glad to see the discussion of DHEA. Swale ( hope he is still here) has a great prospective and is a great resource.. with other moderators.
My belief from study is DHEA is a poor man's HGH. Reviewed studies just emerging.
Someone asked about transdermal Chrysin. I compound it myself, and since I have no way of measuring it, I just look at T to E. As long as that is good, I am cool. Cheap to do too. It is proven to work in vitro... I am trying to find a way to make it work in vivo.
I also use as has been noted Zinc, Cu, C, E ( alt days) and I know (Swale)it is contra indicated but alternating 4-ETAC-3,16,17 Trione and 3,17 DOEC 1,4,6 Triene by days at dose. These are oral and break my non-bioidentical rule, but I am experimenting and have done these about 6 months.
As I said, all I can do is expriment and check the T's and E's. Again, I care less about DHT cept on my head, lol. It won't convert and it is positive for the prostate. Conversely super physiological levels are not for me in the T line... that is a no no. I think that is the reason I an not positive about injections: to get a level one is goona have a period of superphysiological T levels. Has to happen.
My goals: Youth and adolescent libido at middle age. With all the steroidal trans I do watch my cholesterol ( 127) and find fish oil a positive... still working on that one. Rest of the panel is very good and relate that to T levels as most non pharma funded studies indicate. T is a marvelous antidepressant as well.
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
Frank,
Forgive me if you reported back on this, as if you did then I miseed it. But how did your experiment with subq injections work out? Any notable problems? Any rise in E2 as was concerned by some (including SWALE) with doing T sub q? Any notable positive effects?
I stopped doing the T-cypionate injections because they were actually making me feel worse for some reason - even though my baseline T levels were successfully elevated and my estrogens remained perfect (maybe too much depression of the HPA axis?). This was true whether I did IM or subQ. Part of the reason I looked into doing suqQ was to see whether I'd feel better going that route, but there was no difference, i.e., they were both equally bad for me. I think subQ is probably okay, though, as a method of administration and my impression was that it gives a more steady release of T, for what it's worth. There was no rise in E2, at least for the short time I tried subQ: Four days after a 100mg subQ injection, my E2 was 25 (forget the units right now), which was actually down from the original baseline value of 27. That's with no estrogen management.
I'm going to look into transdermal T at some point, but first I'm checking out some adrenal issues to make sure that that's not the primary problem for me.
Frank
I think subQ is probably okay, though, as a method of administration and my impression was that it gives a more steady release of T, for what it's worth. There was no rise in E2, at least for the short time I tried subQ: Four days after a 100mg subQ injection, my E2 was 25 (forget the units right now), which was actually down from the original baseline value of 27. That's with no estrogen management.
Frankwhardy,
How long were you doing SubQ T shots for before you tested your E2 and it came back at 25.
I stopped doing the T-cypionate injections because they were actually making me feel worse for some reason - even though my baseline T levels were successfully elevated and my estrogens remained perfect (maybe too much depression of the HPA axis?)... but first I'm checking out some adrenal issues to make sure that that's not the primary problem for me.
Frank
That's interesting as I definitely DO have adrenal issues - that in fact caused my hypogonadism (or at least caused it to turn it from the long, slow slide into andropause into instant hypogonadism "right now" - like from fully functioning with excellent libido to an absolute zero in erectile functioning and libido in about a two week time period). The hypogonadism wasn't even borderline (Total T of around 140 - 140 in a reference range of 260 - 1000, at age 53).
Additional testing (24-hour Urinary Free Cortisol Tests) found that I had hypercortisolism BIG TIME. Highly elevated cortisol (the first two tests were in range of 5 - 6 times the normal max; test since then have run the range of 1.5 to 2.5 times normal max). On top of that a small tumor was found in my left adrenal gland that was (naturally) initially assumed to be the cause of the hypercortisolism (i.e., a Cushing's Syndrome situation) - but danged if follow-up testing (and let me tell ya', lots and lots of advanced follow-up tests) have revealed tests results that showed it might be Cushing's (maybe 10% of tests), it definitely isn't Cushing's (maybe 70% of tests) or borderline "flip-a-coin" results (the remaining 20%).
Anyway, when you talk about "feeling worse", what specific symptoms do you refer to? When my situation hit (June of 2004) I had a number of symptoms aside from the specific hypogonadal ones. I have found that TRT has helped my symptoms overall, specifically improved the ED (about completely) and the libido (about 75%), but hasn't really done that much for the other symptoms.
But then if those other symptoms are primarily associated with other aspects of the hypercortisolism problem then I should not expect TRT to solve those hypercortisolism issues, eh?
Anyway, I have felt TRT to be a definite aid - in my case - to the overall treatment plan. As has been pointed out to me by a couple different endos, even after they get the hypercortisolism under control (let's say - for example - that it turns out that the tumor is responsible for the hypercortisolism and they resolve it via surgical intervention), chances are that at my age (coming up on 55 now) that my hypogonadal issue would probably NOT resolve and that I'd need to remain on TRT.
And which I understand and have no problem with. Personally I just started SWALE's protocol - using the Test Cyp shots (100mg weekly) and am waiting for the first phase to complete so I can get into the HcG aspect.
Anyway, feel free to PM me if you have any questions concerning the cortisol issue, adrenal gland issues, etc. I have picked the brain of my "Adrenal and Pituitary Gland Specialist" Endo (from a nearby major metro medical center clinic) and am scheduled to go to NIH in Bethesda, MD for a 12-day adrenal gland tumor study in the just over a month.
1cc, I did subQ for only 2 injections (i.e., 100mg/wk) prior to that E2 test.
Larry,
I'm thinking possibly that I'm more in the hypocortisolism area of adrenal problems. The T injections exacerbated my primary symptom of fatigue/tiredness/lack of energy, with the same pattern occurring over and over again with each weekly injection: starting a few hours after a T injection (100mg IM or subQ) I would begin feeling a little better but that would only last a few additional hours, and then by the next morning I would actually feel even more fatigued than my "normal" very fatigued baseline level that has plagued me for several years now. Over a period of 3 or 4 days after the injection my energy levels would then gradually recover back to baseline.
My understanding is that exogenous T can suppress the HPA axis, possibly by a number of different mechanisms, but the one that I remember is that the reduction in LH that occurs can apparently cause a reduction in P450scc activity, the enzyme that converts cholesterol into pregnenolone and the rate-limiting step for the production of cortisol. So I'm guessing that my cortisol levels were getting depressed by the T injections(?). I'm not sure if in that case HCG might possibly work better to boost my T levels, but in the meantime I've added DHEA (25mg/day), which has helped quite a bit with improving my sense of "well being," and I'm going to see what adding pregnenolone does as well (I'm hoping to raise my cortisol levels, especially in the morning, although I'm not sure how effective that exogeneous pregnenolone is in that regard).
Linear Mode
