More testosterone = better gains?

sikdogg · Jun 25, 2006

kcee said:
What is a good level for a guy in his late 40's-early 50's? I had mine checked (50 years old) and the doctor said it was very good ( 550). Is that okay for a guy my age? I still am able to build muscle well, so I guess it is okay? I do have some mild ED and that is why I had it checked. Fortunately, all of the ED drugs seem to work good for me as long as I take them on an empty stomach.
kcee

550 is not bad at all... but without knowing the lab range for you test it's hard to say for sure. Most lab ranges run 350-1000 for Total Testosterone. Your result falls just below the mid so it's good. I don't think any doctor would treat you for low test with that result. Most doctors that treat hypogonadal men (men with low test) aim for getting Total Test levels in the upper 1/3 of the range or somewhere above 700. At this level, you will feel like you're 25 years old again, physically and libido will definitely be up.

Regarding your mild ED... how's your cholesterol levels and blood pressure?? These can affect how your junk works. Also, did you get any other tests done besides Total Testosterone?? like Free Testosterone, DHT, SHBG, Estradiol (E2), LH, and FSH. E2 is very important as it has a huge and direct effect on libido as does Free Test.

fallguy · Jun 25, 2006

Damn, Both times I had mine check I was at 220. The scale was 200 to 1200.

goldmember · Jun 25, 2006

sikdogg said:
550 is not bad at all... but without knowing the lab range for you test it's hard to say for sure. Most lab ranges run 350-1000 for Total Testosterone. Your result falls just below the mid so it's good. I don't think any doctor would treat you for low test with that result. Most doctors that treat hypogonadal men (men with low test) aim for getting Total Test levels in the upper 1/3 of the range or somewhere above 700. At this level, you will feel like you're 25 years old again, physically and libido will definitely be up.

Regarding your mild ED... how's your cholesterol levels and blood pressure?? These can affect how your junk works. Also, did you get any other tests done besides Total Testosterone?? like Free Testosterone, DHT, SHBG, Estradiol (E2), LH, and FSH. E2 is very important as it has a huge and direct effect on libido as does Free Test.

yes and tsh, t3, t4, and prolactin are also important

goldmember · Jun 25, 2006

sikdogg said:
Yes but once you past puberty, your epiphyseal growth-plates close and so does the growth effects of testosterone to male organs and HGH to ones height. This is basic male endocrinology and has been proven study after study after study...

I think test's penile growth effects wear off after puberty because of androgen receptor down-regulation, after a few years of high exposure. Theoretically, if you can up-regulate androgen receptors in the penis, you can spur growth with test (if this theory is true). Prostaglandin E-1 is one substance known to upregulate androgen receptors. Bodybuilders who locally inject pge1 notice the area grow much faster than other body parts, and it makes the following steroid cycle very effective when working that specific area even after discontinuing the pge1.

sikdogg · Jun 26, 2006

goldmember said:
I think test's penile growth effects wear off after puberty because of androgen receptor down-regulation, after a few years of high exposure. Theoretically, if you can up-regulate androgen receptors in the penis, you can spur growth with test (if this theory is true). Prostaglandin E-1 is one substance known to upregulate androgen receptors. Bodybuilders who locally inject pge1 notice the area grow much faster than other body parts, and it makes the following steroid cycle very effective when working that specific area even after discontinuing the pge1.

I've never heard of bodybuilders site injecting PGE1... PGF2a, yes but never PGE1.

sikdogg · Jun 26, 2006

goldmember said:
yes and tsh, t3, t4, and prolactin are also important

Yes, i agree...

sikdogg · Jun 26, 2006

goldmember said:
I think test's penile growth effects wear off after puberty because of androgen receptor down-regulation, after a few years of high exposure....

That theory has actually been de-bunked... If an adolescent's AR down-regulates it does so at the same time as that the epiphyseal growth-plates close. An adult male's AR does not down-regulate after years of high exposure. This is proven everyday by professional bodybuilders who routinely take several grams of AAS per week for 10 years or more. If that was the case, no professional bodybuilder could continue to make gains year after year.

sikdogg · Jun 26, 2006

fallguy said:
Damn, Both times I had mine check I was at 220. The scale was 200 to 1200.

If you are experiencing symptoms of low testosterone, then your doctor should be putting you on TRT. Go to All Things Male and download Dr. Crislers paper TRT: A Recipe for Success. Read it and show it to your doctor. If he still won't treat you then you need to find a new doctor.

Also download American Association of Clinical Endocrinology's (AACE) guide on Hypogonadism. Some items it discusses like HCG application a little dated but it's very good reading.

goldmember · Jun 26, 2006

sikdogg said:
That theory has actually been de-bunked... If an adolescent's AR down-regulates it does so at the same time as that the epiphyseal growth-plates close. An adult male's AR does not down-regulate after years of high exposure. This is proven everyday by professional bodybuilders who routinely take several grams of AAS per week for 10 years or more. If that was the case, no professional bodybuilder could continue to make gains year after year.

Receptors can down-regulate locally. It is possible that they down-regulate in the smooth muscle (CC) while up-regulating in the skeletal muscle.

Why would the AR's need to D-R at the same time as the epiphyseal plates close...?

sikdogg · Jun 26, 2006

goldmember said:
... Why would the AR's need to D-R at the same time as the epiphyseal plates close...?

I'm not necessarily saying that they do but speculate that the closure of the epiphyseal plates is part of a larger physiology change that takes place which effect how hormones affect the body. It is sort of a demarcation point from which testosterone no longer exerts its effects on genitals and GH no longer exerts its effect on growth. I don't pretent to fully understand the whole metabolic process that happens when one passes puberty, just guesses from past study. I could be way off base...

goldmember · Jun 28, 2006

I am researching this epiphyseal plate closure, specifically the physiological differences between a "closed" and "open" plate.

I am beginning to see the logic behind your assumption that the AR in the penis D-R at ,or near, the same time as the E.P. closure occurs. ie both would theoretically require prolonged exposure to androgens.

However, you must also consider that female adolescents' E.Ps close prior to the age that a male adolescent's EPs close, and androgen levels in females are much much lower. Also, it can't be assumed that smooth muscle tissue experiences D-R of ARs in the presence of the same level of androgens required to close EPs, because it seems so far that the mechanism for closure of the EPs is independant of AR levels (but still dependant on androgens themselves in some eluding way--that I will find out shortly). I will fill you in with the details as soon as I find them out.

sikdogg · Jun 28, 2006

I totally agree with you...

goldmember said:
... it seems so far that the mechanism for closure of the EPs is independant of AR levels (but still dependant on androgens themselves in some eluding way--that I will find out shortly). I will fill you in with the details as soon as I find them out.

I believe you will find that the closure of EPs is dependent on estrogen... so they are indirectly dependent on androgens in males. I will try to find the study where i read this from.

sikdogg · Jun 28, 2006

Here's a few that i was able to dig up... they're pretty easy to find actually.

Clin Calcium. 2006 Mar;16(3):450-4. Related Articles, Links

[Excessive androgens and short stature in childhood]

[Article in Japanese]

Matsuo K, Fujieda K.

Asahikawa Medical College, Department of Pediatrics.

Sex steroids play important role for bone maturation and statural growth in childhood, especially puberty. The closure of epiphyseal growth plate cartilage is regulated mainly by estrogens. Aromatization of androgens to estrogens is working in men as well as women. Thus, androgens are directly related to epiphyseal growth and maturation. In clinical conditions such as precocious puberty, excessive androgens production occurs in prepubertal period. This advances bone maturation as well as pubertal change resulting in short stature because of premature closure of epiphyseal growth plate. Various causes of precocious puberty are now identified.

Publication Types:
Review

PMID: 16508127 [PubMed - indexed for MEDLINE]

Mol Cell Endocrinol. 2006 Jun 9; [Epub ahead of print] Related Articles, Links

Use of aromatase inhibitors to increase final height.

Dunkel L.

Kuopio University Hospital, Kuopio, Finland.

During puberty in both sexes, the mechanism involved in epiphyseal fusion is mediated by the action of estrogen through a cascade of events including proliferation, differentiation, and apoptosis of chondrocytes. The enzyme P450 aromatase catalyzes the aromatization of C(19) androgens (androstenedione and testosterone) to C(18) estrogens (estrone and estradiol). Inhibition of estrogen action by aromatase inhibitors (AIs) appears to decelerate the process of growth plate fusion, and thus AIs may be used therapeutically to increase adult height. The clinical experience with AIs in the pediatric setting is limited to testolactone, fadrozole, letrozole, and anastrozole. Testolactone, a nonselective steroidal AI, has been used successfully as an adjunct to antiandrogen and gonadotropin-releasing hormone analogue (GnRHa), therapy for children with familial male-limited precocious puberty (FMPP) and congenital adrenal hyperplasia (CAH), and with some success in girls with McCune-Albright syndrome. The limitations of testolactone include its relatively low potency and the need for frequent dosing. Results of a randomized placebo-controlled trial in boys with delayed puberty treated with letrozole, a selective nonsteroidal AI, found that boys treated with letrozole+testosterone experienced delayed bone maturation and good growth response and achieved an increase in predicted adult height. In this study, only minor differences in bone density were seen between the placebo and letrozole treatment groups, both of which were receiving concomitant testosterone therapy. No adverse effects on testis size or inhibin B concentration were noted. The therapeutic value of AIs in growth promotion now remains to be substantiated in future controlled clinical trials.

PMID: 16766117 [PubMed - as supplied by publisher]

Pediatr Endocrinol Rev. 2006 Apr;3 Suppl 2:301-5. Related Articles, Links

Mechanisms for delaying epiphyseal fusion and improving adult height in pubertal patients with hypopituitarism.

Eugster EA.

Section of Pediatric Endocrinology, Department of Pediatrics, James Whitcomb Riley Hospital for Children, Indiana University School of Medicine, Indianapolis, Indiana.

The preservation of linear growth potential is an important goal for many patients presenting to the pediatric endocrine clinic. This is particularly true for pubertal adolescents with growth hormone deficiency who are diagnosed late and for short children with hypopituitarism and central precocious puberty, a combination that confers a poor prognosis for adult stature. In this review, currently available and promising new strategies for delaying epiphyseal fusion and increasing adult height in pubertal patients are discussed. While GnRH analogues are the standard of care for treating central precocious puberty, concerns exist regarding adverse metabolic effects of these agents when used in adolescence. Alternate approaches that diminish epiphyseal estrogen exposure yet allow pubertal development to progress in boys include antiestrogens in the form of aromatase inhibitors and estrogen receptor antagonists. Data from clinical trials using these compounds in a variety of pediatric conditions are summarized, and future directions are identified.

PMID: 16675928 [PubMed - in process]

goldmember · Jul 7, 2006

Great studies SD.

This would explain why highly anabolic and zero androgenic steroids cause INCREASED bone growth, while the more androgenic the steroid, the more it prematurely closes EP's. Highly androgenic steroids rapidly convert into estrogens, while anabolic steroids do not convert very readily.

sikdogg · Jul 7, 2006

I'm not sure if i agree... DHT is the most androgenic hormone in the male body but it also acts as an aromatase inhibitor... DHT directly inhibits estrogens activity on tissues. It either does this by acting as a competitive antagonist to the estrogen receptor or by decreasing estrogen-induced RNA transcription at a point subsequent to estrogen receptor binding.

Second of all, DHT and its metabolites have been shown to directly block the production of estrogens from androgens by inhibiting the activity of the aromatase enzyme. The studies done in breast tissue showed that DHT, androsterone, and 5alpha-androstandione are potent inhibitors of the formation of estrone from androstenedione. 5alpha-androstandione was shown to be the most potent, while androsterone was the least.

J Steroid Biochem Mol Biol. 2006 Feb;98(2-3):133-8. Epub 2005 Dec 28. Related Articles, Links

Aromatase-independent testosterone conversion into estrogenic steroids is inhibited by a 5 alpha-reductase inhibitor.

Ishikawa T, Glidewell-Kenney C, Jameson JL.

Division of Endocrinology, Metabolism, and Molecular Medicine, Northwestern University Feinberg School of Medicine, Galter Pavilion, Suite 3-150, 251 E. Huron St., Chicago, Illinois 60611-2908, USA.

Estrogens are generated mainly by the action of aromatase, which converts testosterone to estradiol and androstenedione to estrone. However, in addition to estradiol and estrone, a variety of other steroids, whose synthesis is not dependent on aromatase, can stimulate the estrogen receptor. Here we show that testosterone is converted into such estrogenic steroids by aromatase-negative HeLa cells. This aromatase-independent generation of estrogenic steroids is seen in aromatase-positive MCF-7 cells as well. In both cell lines, the synthesis of estrogenic steroids was blocked by inhibition of testosterone conversion into dihydrotestosterone using a 5 alpha-reductase inhibitor finasteride, suggesting that they are generated downstream of dihydrotestosterone. This finding raises the possibility that the combination of a 5 alpha-reductase inhibitor and an aromatase inhibitor may reduce estrogenic steroids in vivo more completely than an aromatase inhibitor alone.

PMID: 16386416 [PubMed - indexed for MEDLINE]

goldmember · Jul 8, 2006

sikdogg said:
I'm not sure if i agree... DHT is the most androgenic hormone in the male body but it also acts as an aromatase inhibitor... DHT directly inhibits estrogens activity on tissues. It either does this by acting as a competitive antagonist to the estrogen receptor or by decreasing estrogen-induced RNA transcription at a point subsequent to estrogen receptor binding.

Second of all, DHT and its metabolites have been shown to directly block the production of estrogens from androgens by inhibiting the activity of the aromatase enzyme. The studies done in breast tissue showed that DHT, androsterone, and 5alpha-androstandione are potent inhibitors of the formation of estrone from androstenedione. 5alpha-androstandione was shown to be the most potent, while androsterone was the least.

This study seems to be suggesting that DHT upregulates the conversion of test-->estro....

If taking a 5alpha-reductase inhibitor along with an AI lowers estrogen levels, this is saying that LOWER levels of DHT means LOWER levels of estrogen. Correct me if I misinterpreted what you said, but it seems to be the opposite of what you said...

Also, when I said "the most androgenic steroids are the most aromatizable" I was referring to testosterone derivatives, not DHT. I should have been more clear. While DHT and its derivatives are far more ANDROGENIC than testosterone or its derivatives, it cannot be converted into estrogen.

sikdogg · Jul 8, 2006

goldmember said:
This study seems to be suggesting that DHT upregulates the conversion of test-->estro....

If taking a 5alpha-reductase inhibitor along with an AI lowers estrogen levels, this is saying that LOWER levels of DHT means LOWER levels of estrogen. Correct me if I misinterpreted what you said, but it seems to be the opposite of what you said...

Actually i think it says that the test-to-estro conversion was blocked by the inhibition of test-to-DHT conversion by using a 5-AR inhibitor... now i'm a little lost. Maybe your theory was right...

Also, when I said "the most androgenic steroids are the most aromatizable" I was referring to testosterone derivatives, not DHT. I should have been more clear. While DHT and its derivatives are far more ANDROGENIC than testosterone or its derivatives, it cannot be converted into estrogen.

Gotcha... i assumed when you mentioned "the most androgenic steroid..." you meant DHT. My bad...

player89 · Jul 8, 2006

Yo sikdog I been noticing that you have alot of knowledge about the body and was wondering where did you educate yourself.

sikdogg · Jul 8, 2006

From studying anabolic steroids and bodybuilding and how they effect my body... i would never put anything in my body without first knowing how it will affect me today and possibly down the road.

goinfor11x7 · Jul 8, 2006

Is there any way to raise your Test. levels naturally without taking Test. supplements? My urologist has me on a med. to shrink my prostate which is two and half times the normal size. So I hardly need worry about raising my Test. levels when the doc. wants to lower them. I hope Kcee thinks about this before trying to raise his Test. levels being that he's into his 50's now.

I asked the doc. if the med. would shrink my penis as well. He just stared at me. Not very enlightened about discussing these matters. Oh, how I wish I had my old urologist back!!!

<

More testosterone = better gains?

1

0

0

0

1

1

1

1

0

1

0

1

1

0

1

0

1

0

1

0

Similar threads