MESO-Rx
Anabolic Steroids
Injecting testosterone subcutaneously
- Thread starter frankwhardy
- Start date
RitchieC said:
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?
RitchieC said:
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?
SPE said:
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?
Larry
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.
Fun stuff.
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.
Fun stuff.
frankwhardy said:
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?
Thanks.
Larry
frankwhardy
New Member
Hi Larry,
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 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
frankwhardy said:
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.
Larry
frankwhardy
New Member
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).
Good luck with your NIH study.
Frank
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).
Good luck with your NIH study.
Frank
frankwhardy said:
First of all, have you actually had cortisol levels tested? Treating cortisol problems based on how you feel is worse than treatting TRT problems strictly based upon how you feel. And if you are doing testing by way of anything other than 24-hr UFCs then you are NOT getting accurate results. When I talked my first Endo into running cortisol testing on me (I assumed blood or salivary would be done but he was at least smart enough to do 24-hr UFCs), I was totally positive that I was going to come back with Adrenal Fatigue (low levels of cortisol, etc.). You could have knocked me over with a feather when I saw how ELEVATED my levels were.
Also, all of my information - and I haven't studies hypocortisolism that much - have shown just the opposite of what you indicate. It is hypercortisolism that disrupts the HPT Axis, not testosterone disrupting the HPA Axis. The HPA Axis does become dsyfunctional which causes the continued elevated secretions of cortisol, but as the cortisol gets more and more greedy it begins robbing the other hormones of raw material to continue making more and more cortisol.
There's a lot of technical aspects as you're aware, but here's some brief info with attached links for further information (trying for a mix of technical articles and more layman oriented):
http://www.postgradmed.com/issues/1998/07_98/schmidt.htm
the cortisol excess of Cushing's disease may result in secondary hypogonadism by inhibiting secretion of luteinizing hormone and follicle-stimulating hormone.
http://www.nutrition4health.org/NOHAnews/NNW02HardingAging.htm
Conditions which require large amounts of cortisol create a drain on our capacity to produce adequate hormones. To provide the excess cortisol needed to respond to conditions such as pain and inflammation, the body diverts the production of our sex hormones into the production of cortisol. In particular, the body "cannibalizes" our (WOMEN'S) sex hormone progesterone to make additional cortisol... This decrease in our progesterone often leaves us with low progesterone in comparison to our estrogen or testosterone and leads to conditions of "estrogen dominance" (definitely is doing the same thing with testosterone in men - LRS)
http://www.gsdl.com/home/assessments/malehormone/appguide/index3.html
Secondary hypogonadism can develop as a result of hypothalamic or pituitary disease, obesity, hypothyroidism or other causes. Some conditions, such as hypercortisolemia... and severe systemic illnesses, can trigger hypogonadism through a combination of both primary and secondary mechanisms.
http://www.wellmax.org/NewsPub/Stories/2001/05/07/9892607709.html
Hyperprolactinemia, hypercortisolemia, or hypothyroidism are also common. [85] Many of the acquired causes of primary adult hypogonadism are rare but need to be considered when taking a medical history. These include mumps orchitis, occupational exposures, radiation to the testes, cancer chemotherapy, excessive heat exposure of the testes, interruption of blood flow to the testes secondary to surgery, hemochromatosis, adrenal or testicular tumors that produce estrogens
http://www.google.com/answers/threadview?id=450553
According to the Great Smokies Diagnostic Lab, these are the causes of
hypogonadism: chronic/systemic illness, surgery, chemotherapy... premature aging, testicular trauma, severe stress, Kleinfelter's syndrome... sleep apnea, hypercortisolism... hyperthyroidism and malnutriton
http://neoteny.info/a/testosterone.html
Two mechanisms can account for a lower gland production of the hormone: -- a persisting significant rise in the levels of circulating epiniphrine could induce a drop in the plasma levels of testosterone by means of reduced testicular production, with unchanged global metabolic clearance (32); --- hypercortisolemia, under the condition that it is prolonged enough, would reduce the plasma levels of testosterone (33,34). This normal profile (hypercortisolemia, hypotestosteronemia) is described in other stress conditions (35,36) and in Cushings's syndrome (37,38,39).:
http://www.aace.com/pub/ep/199905ep.php
The pathophysiologic features of glucocorticoid-induced hypogonadism and the possible relationship to the muscle atrophy in patients receiving glucocorticoids were assessed... One of the contributing factors in the development of muscle atrophy is hypogonadism that is induced by long-term glucocorticoid use (or production) - Note glucocorticoid refers to the trechnical term of cortisol in the body - LRS
http://www2.mcdaniel.edu/Biology/EPS04/stress/stress.html
Similarly, cortisol and related glucocorticoid hormones not only inhibit the release of GnRH, but also the release of luteinizing hormone, which prompts ovulation and sperm release. Glucocorticoids also inhibit the testes and ovaries directly, hindering production of the male and female sex hormones testosterone, estrogen, and progesterone.
http://www.isisboston.com/Treatmentroom/glands.htm
Cortisol is catabolic and is anti-inflammatory, immuno-suppressive and helps to regulate glucose production. It redirects blood to somatic muscles for the fight or flight response and also inhibits the thyroid by increasing thyroid-binding proteins made in the liver. It influences the activity of DHEA and testosterone.
http://www.intense-training.com/archive/t-21137.html
Testosterone levels are decreased with:
Male hypogonadism and
Men with Cushing's disease or those receiving glucocorticoid therapy.
And BTW, if you legitimately have definitely low levels you should be seeking treatment from an Endo (preferably a specialist in Adrenal Gland Disorders). Sub normal cortisol levels are beyond simply "adrenal fatigue". Adrenal shock can result with fatal results.
Larry
frankwhardy
New Member
Thanks, Larry. Yes, I saw an Endo a few days ago. He's wanting me off everything, including the testosterone (which I'd stopped anyway since it was seemingly making matters worse - at least in the form of T-cyp), for 3 months and then do bloodtesting to check baseline levels of everything at that point. On the lab slip that he gave me (to use in 3 months) he didn't check the box for 24 hr UFC and I'm tempted to go ahead and write it in myself and hope he won't remember not ordering it. 
When I went in to see him I was actually initially thinking that I might be producing too much cortisol, but the Endo indicated that I just didn't have the bodily features of someone with Cushing's (i.e., no fatty hump between the shoulders, or round face, etc.). My blood pressure also runs on the normal to low side. I do have what has become a permanently reddened face and neck (what for me would pass as a tan - except that I never get any sun exposure), and so the Endo is thinking a hypocortisol situation, if anything. Do you have the classic hypercortisolism signs?
This hormonal business is very tricky because many of the exact same symptoms can be caused by either of an excess or a deficiency of the very same hormone.
Frank
When I went in to see him I was actually initially thinking that I might be producing too much cortisol, but the Endo indicated that I just didn't have the bodily features of someone with Cushing's (i.e., no fatty hump between the shoulders, or round face, etc.). My blood pressure also runs on the normal to low side. I do have what has become a permanently reddened face and neck (what for me would pass as a tan - except that I never get any sun exposure), and so the Endo is thinking a hypocortisol situation, if anything. Do you have the classic hypercortisolism signs?
This hormonal business is very tricky because many of the exact same symptoms can be caused by either of an excess or a deficiency of the very same hormone.
Frank
Frank,
You can have a Cortisol Saliva Test done which would be the most accurate to ascertain whether your adrenals are producing sufficient cortisol. Saliva samples are taken at 4 different times of the day, and it will show what time of day you are most deficient.
http://www.metametrix.com/TestServ/default.asp?PageID=21&TabID=25
This is the cheaper one and it's all you need:
#0243 - Adrenal Stress (Cortisol and DHEA Only)
You can have a Cortisol Saliva Test done which would be the most accurate to ascertain whether your adrenals are producing sufficient cortisol. Saliva samples are taken at 4 different times of the day, and it will show what time of day you are most deficient.
http://www.metametrix.com/TestServ/default.asp?PageID=21&TabID=25
This is the cheaper one and it's all you need:
#0243 - Adrenal Stress (Cortisol and DHEA Only)
frankwhardy
New Member
Thanks 1cc, that's a good idea. I'd been thinking about using ZRT Laboratories for that multiple-time cortisol testing (I've had pretty good success with them in the past with other tests).
Frank
Frank
frankwhardy said:Thanks, Larry. Yes, I saw an Endo a few days ago. He's wanting me off everything, including the testosterone (which I'd stopped anyway since it was seemingly making matters worse - at least in the form of T-cyp), for 3 months and then do bloodtesting to check baseline levels of everything at that point. On the lab slip that he gave me (to use in 3 months) he didn't check the box for 24 hr UFC and I'm tempted to go ahead and write it in myself and hope he won't remember not ordering it.
When I went in to see him I was actually initially thinking that I might be producing too much cortisol, but the Endo indicated that I just didn't have the bodily features of someone with Cushing's (i.e., no fatty hump between the shoulders, or round face, etc.). My blood pressure also runs on the normal to low side. I do have what has become a permanently reddened face and neck (what for me would pass as a tan - except that I never get any sun exposure), and so the Endo is thinking a hypocortisol situation, if anything. Do you have the classic hypercortisolism signs?
This hormonal business is very tricky because many of the exact same symptoms can be caused by either of an excess or a deficiency of the very same hormone.
Frank
Frank,
I have NONE of the Cushing's signs either. Actually there are multiple forms of Cushing's. Cushing's simply refers to having hypercortisolism. Cushing's Syndrome is caused by an adrenal gland tumor or an ACTH-secreting small cell cancer. Cushing's Disease is caused by a pituitary gland tumor. The you have a form of Cushing's that is caused by excessive use of artificial cortisol (like people who take prednisone for arthritis, etc.). And then there's Pseudo Cushing's which is the combined forms of every other cause. It could be acute alcoholism. It could be from acute or chronic anxiety or depression. It could be from AIDS or HIV. With Pseudo Cushing's (which is a horrible name as many people think that a PS diagnosis means that they don't have hypercortisolism), it is quite frequent that many of the physical manifestations do NOT appear. And even with regular Cushing's patients, there are many individuals who simply do not - especially in the early stages - develop the physical manifestations. They may, for example, have the elevated cortisol primarily attacking their neurotransmitters and HPT axis, so they have primarily problems with anxiety and hypogonadism. Another may have the elevated cortisol causing problems with severe depression, cardivascular problems - aside from BP, and extreme bruising and wound healing. The examples go on and on.
Anyway, I do NOT have the bodily features of someone with Cushing's, i.e., no fatty hump between the shoulders ("buffalo hump"), or round face ("moon face"), or reddened face, or severe torso obesity with thin arms and legs, etc. My blood pressure ALSO runs on the normal to low side (unless I happen to be on a particular medication here or there which raises it). And yet my first two 24-hr UFC cortisol tests showed cortisol levels in the range of 5 - 6 times the normal max. And the ones since then have been 1.5 to 2.5 times the max.
RE: "I do have what has become a permanently reddened face and neck"
Frank, I find that comment very interesting. The darkened pigmentation feature of Addision's Disease (extremely low levels of crotisol) isn't from sun exposure or a form of tanning, it is an actual pigmentation coloring change of the skin. And it is usually all across the body. And it very definitely is a brown coloring. Not red or reddened. And yet "red faced" (as well as "moon faced" or extremely "chubby faced") is definitely one of the physical manifestations of hypercortisolism. In fact, I do have that one to a slight extent come to think of it. Also, I have noticed that TRT has NOT cured my various ills - simply because hypogonadism was only one feature that hypercortisolism brought on. There are days when I feel "not too bad" and then days when I feel "exceptionally worse", (the actual phases of hypercortisolism run in cycles due to the cyclic nature of the cortisol secretions)... possibly you had a similar situation where you just thought it was connected to the TRT?
Also, trust me on the 24-hr UFC. If your doctor is not having that test run, I personally (now, with all my experiences over the last 18 months) would have to be concerned about his expertise in this one particular area. Yes, that one particular salivary test that is done 4x a day (like every six hours) "may" be sufficient to let you know whether or not your are producing insufficient amounts, but neither it nor any serum test (unless they have you in the hospital and are doing draws every 30 minutes) are going to let you know if you are elevated into hypercortisolism. Personally, I'd call the endo and tell him your concerns and simply tell him that you'd like to add the 24-hr UFC to the Labs "just to be on the safe side". Being a urinary test it's actually a relatively inexpensive test - and I can't see how he would have a problem with it.
As a last point in that regard, if you have read SWALE's actual protocols for his TRT, if you go to the opening section where he talks about the Labs that he does, you will note that he references doing urinary cortisol tests for the most accuracy... well, he's referring to the good old 24-hr UFC.
If you don't have his protocol a copy of it can be viewed (and even downloaded and printed out) at: http://www.allthingsmale.com/
Specific document at: http://www.allthingsmale.com/word_docs/TRT.doc
CORTISOL
True Anti-Aging medicine must be well-familiarized with the ins and outs of this hormone, the only one our bodies cannot live without. Elevated levels can cause secondary (hypogonadotrophic) hypogonadism. I try controlling elevated cortisol with Phosphatidylserine, 300mg QD, with good results. It is just as important to watch for depressed cortisol levels, as well. The assay of choice for that condition is a 24-hour urine.
Note: Phosphatidylserine (and relora and holy basil extract and a few other OTC supps) can be of benefit in cases of mildly elevated cortisol or if you have consistent high normal levels cortisol from daily stress, etc. But none of them will work for an actual medical condition of hypercortisolism - no matter what the cause.
Anyway, Frank, I wish you well in your diagnostic efforts. Both hypercortisolism and hypocortisolism are quite serious disorders, so I hope that your levels in that particular hormonal testing are excellent. Please keep me updated on your results - so I'll know when to uncross my fingers!
Larry
1cc said:
This now seems to make more sense considering that the following studies seem to indicate that it is the large area of skin that T Gels/Creams are applied to that determines how much of it will be converted to Estrogen or DHT. The smaller the area of Skin, the less is converted to Estrogen and DHT.
In the case of SubQ T injections, it is injected into a tiny spot under the skin and is released slowly, which seems to me to be exactly how pellets work, and pellets are known for the least conversion to Estrogen.
Here are some more studies that seem to suggest that a smaller application area for Testosterone Gel/Cream should lead to lower DHT and Estrogen conversion.
https://thinksteroids.com/community/posts/450206
Matt Muscle
New Member
Yes.. i know a couple of guys on Pellets and they are having no problems at all with Estrogen. The very stable levels of T seem to make them feel much more consistent.1cc said:
Injecting just once a week still creates the problem of surging T levels although much reduced as compared to forghtnightly injections. The subcut method certainly looks like it "could" further help this problem.
According to this post Dr. Shippen has his patients do SubQ T Cyp injections every 3 days. This would play a big part in further stabilising the T blood levels, and the fact that it's SubQ makes it a lot easier to deal with. A lot of body builders already do T Cyp shots IM every 3 days in order to stabilise their blood levels. I recently switched to T Cyp shots every 3 days and am considering doing the shots SubQ. My initial concern was excess aromatization, but this is starting to look more and more unlikely, and rather the opposite may be true.
https://thinksteroids.com/community/posts/441001
https://thinksteroids.com/community/posts/441001
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