Muscle injuries despite high T and IGF-1
- 04-29-2011, 03:17 AM
Muscle injuries despite high T and IGF-1
I am 49 and in recent years seem to be prone to muscle injuries with very poor recovery. To be more specific it all started with a single run of 16 miles which was double what I had been doing in training at the time but I was in fantastic shape. This overdone workout trashed my anterior tibialis muscles. It took me over one year to recover and never to 100%. Another overdone workout (although to much less of an extent) resulted in a relapse of the first injury and the same problem affecting the calf muscles. This took another year and even less full recovery. Now I am always on the verge of relapsing and cannot increase my training very much. In addition, I hit my thigh on a car bumper and that also became a serious injury way out of proportion to what you would expect. Nothing seems to heal anymore.
I had some lab work done to try to understand the problem. Here are the results (and reference ranges) from Quest:
T3, Free 3.3 (2.3-4.2 pg/mL)
T4, Free 1.5 (.8-1.8 ng/dL)
TSH (high sensitivity) 1.54 (.40-4.50 mIU/L)
FSH 4.6 (1.6-8.0 mIU/mL)
LH 3.7 (1.5-9.3 mIU/mL)
Progesterone 0.5 (<1.4 ng/mL)
E2 (not sensitive) 42 (<52 pg/mL)
Cortisol, AM 18.7 (4-22 mcg/dL)
Testosterone 929 (250-1100 ng/dL)
Free Testosterone 110.6 (35-155 pg/mL)
SHBG 72 (9-45 nmol/L)
Insulin <2 (<17uIU/mL)
IGF-1 288 (50-303 ng/mL)
DHT 19 (25-75 ng/dL)
DHEA 489 (61-1636 ng/dL)
Testosterone looks pretty good to me as does IGF-1. I'm taking Avodart which explains the slightly low DHT. I've never taken any other anabolics or related drugs. SHBG is very high but my free Testosterone still seems OK. DHT on the lower side is not associated with muscle issues and there are no receptors for DHT on muscles so it doesn't seem like that would explain it. I'm more suspicious of estrogen as I have some symptoms associated with poorly regulated E2 as well. My E2 test was not sensitive so probably not accurate. Anybody with similar issues/profile? Any ideas about what might explain the problems?
- 04-30-2011, 01:34 PM
Muscle may not have DHT receptors, but it is more anabolic than testosterone and interacts directly with the CNS.
05-01-2011, 10:23 PM
Thank you for the reply DragonRider.
I have noticed that there are mixed views on the importance of DHT. The medical literature tends to discount its value. There is a rare medical condition where men do not make DHT. I'm not aware of any problems these men have. One problem that they don't have is that they never suffer from an enlarged prostate. My father suffered a lot from BPH and it hardly deserves to be called benign. PSA is a better predictor of BPH than it is of prostate cancer. After having my PSA checked and finding myself in the high risk group I decided to start taking Avodart in hopes of avoiding my father's fate.
My experience with Avodart is quite different from a lot of what I've seen on these boards and elsewhere. I can only conclude that men are more diverse with regard to these hormonal issues than I expected. I see a lot of men saying that they need DHT for their libido and erectile function. Clinical trials with Avodart reported that many men experienced negative impacts on their sex life but that this was transient after 1 year. A much smaller percentage of men reported the opposite effect. I fall into this category. Things were not bad for me before but lowering DHT actually helped me. Another very noticeable benefit for me was that at the time I was starting to experience thermo-regulation issues which I would guess was hormonally related. That got much better after taking Avodart as well. I noticed no downsides except a very minor nipple tenderness that lasted about a week in the beginning. It seemed like a wonder drug.
Perhaps for me the muscle repair issue is a downside for lower DHT but I'm not inclined to think this is a direct effect. I searched very hard for such a connection in the literature and elsewhere and could find nothing about this. There must be many thousands of men on this drug so you would think someone would have noticed a problem like this by now.
The relationship between DHT and SHBG is also unclear to me. SHBG is supposed to be lowered by androgens in general and DHT is in this category. One paper I found showed little effect of DHT on SHBG but this was a short term study as I recall. On the other hand, Proviron, which is a DHT analog has very strong SHBG lowering effects. By blocking testosterone to DHT conversion you will raise testosterone and this in turn would increase estrogen. So you would expect by this indirect mechanism that Avodart should increase SHBG. I don't understand why the literature is not more clear on this.
At this point I inclined to suspect estrogen as the culprit. High estrogen does increase SHBG. I really do need the sensitive test to find out where I stand on this. The problem with blaming estrogen is that while I have found a connection between estrogen and muscle repair it seems that more is generally good. The data I have seen is very limited though. I have not seen a connection made between high estrogen and muscle repair problems. I have a genetic condition that up-regulates certain estrogen responsive genes that could explain my situation but not enough is known about this to be sure. Nevertheless, it makes estrogen the most likely culprit.
05-02-2011, 01:33 AM
5-alpha-reductase type 2 deficiency (5-ARD) is an autosomal recessive sex-limited condition resulting in the inability to convert testosterone to the more physiologically active dihydrotestosterone (DHT). Because DHT is required for the normal masculinization of the external genitalia in utero, genetic males with 5-alpha-reductase type 2 deficiency are born with ambiguous genitalia (ie, 46,XY disorder of sex development).
Patients with 5-alpha-reductase type 2 deficiency usually present with striking ambiguity of the genitalia, with a clitoral-like phallus, severely bifid scrotum, pseudovaginal perineoscrotal hypospadias, and a rudimentary prostate. Occasionally, patients can appear more masculinized; they may lack a separate vaginal opening, have a blind vaginal pouch that opens into the urethra, and have isolated penile hypospadias or even a penile urethra.
The uterus and fallopian tubes are absent because of the normal secretion of the müllerian-inhibiting factor. Testes are intact and are usually found in the inguinal canal or scrotum; however, cryptorchidism is frequently described with testes occasionally located in the abdomen. Wolffian duct differentiation is normal with seminal vesicles, vasa differentia, epididymides, and ejaculatory ducts. The prostate is small, nonpalpable, and rudimentary in adulthood. Neither benign prostate hyperplasia (BPH) nor prostate cancer has been reported in these patients.
05-02-2011, 03:51 AM
Thanks for finding that article DragonRider. It jogged my memory - I did know that DHT is important for development.
08-08-2011, 02:20 PM
Androstenedione 164 ng/dL (40-190 ng/dL)
Prolactin 7.8 ng/mL (2-18 ng/mL)
DHEA-S 239 mcg/dL (45-345 mcg/dL)
So it seems that DHT is the key regulator of SHBG levels for my case. A while ago I stopped Avodart for a month and it did not provide any immediate benefit. With these results I decided to cut my Avodart dose in half for a longer period of time to see if that is helpful. The remaining question is whether I should try to use a very low dose anti-estrogen to bring down E2 a little. Suggestions?
08-08-2011, 02:31 PM
08-09-2011, 03:56 AM
08-22-2011, 08:13 PM
I saw in one of your earlier posts that you had issues with muscle twitch. This is also characteristic of my muscle problems. I believe that you figured out the cause of this for yourself. Can you please tell me what you learned about that?
08-23-2011, 10:13 AM
08-27-2011, 10:44 PM
08-31-2011, 11:29 PM
09-02-2011, 10:30 PM
This thread continues on another thread called "Free estrogen testing".
Last edited by hitest; 11-06-2011 at 11:26 PM. Reason: Added pointer to thread continuation.
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