T Nation

Keeping your Testes Young


#1

Don't post much, but thought ya'll may find this interesting.

And I know animal studies don't always transfer to humans, but it's worth a thought.

http://www.ergo-log.com/continuous.html


#2

A chick the other day mentioned that my testicles don’t look a day over 25…I guess it does work. :slight_smile:


#3

I remember a poster recently suggesting something similar - in that the testes have x capacity to produce test in a lifetime, and periods suppressed ‘saved’ this production so was it possible to produce more after being suppressed for a duration - as one’s balls would need to ‘catch up’ on production i guess…

The study leaves a lot to be desired. It seems too easy and doesnt really ring true with everything else we know about hormone production/synthesis…

What do you think as an educated man WHB?


#4

I was trying not to think about it-and only wanted to generate a chuckle. Oh, well. :slight_smile:

Well…I don’t know that I’m qualified to give a great answer. I luckily remembered an article Cy Wilson had written a number of years ago that touches on the subject. Here is that portion of the article:
[b]
Research Update #4 More Anastrozole News

The update is actually derived from one of the same studies mentioned above. In it (double-blind, placebo-controlled and randomized), they took both 31 young (ages 18-33) and 20 older (60-76) healthy males and gave them 10 mg/day of anastrozole for five days.

They then measured serum concentrations of LH, Testosterone, SHBG and the molecular ratio of Testosterone to SHBG. What they found was that the older men had a diminished response to the aromatase inhibitor in terms of LH pulse amplitude and frequency, as well as total Testosterone and the Testosterone/SHBG ratio.

The authors, based upon this study and a good deal of previous data, concluded that the two most likely causes for such results are:

1) An impairment of GnRH release/secretion from the hypothalamus or some sort of impairment in the ability of GnRH to reach the gonadotropic cells of the anterior pituitary.

2) Impairment of steroidogenesis in the leydig cells as evidenced by a reduced responsiveness to recombinant LH, hCG, as well as estrogen antagonists and GnRH in terms of endogenous Testosterone production. 

Now, whether this impairment at the leydig cells is G protein-coupled receptor-mediated or whether the defect is post receptor-mediated with the defect occurring downstream somewhere, is an important question. I tend to believe itâ??s the former.

In any event, this provides the perfect opportunity for use of a compound which works directly at the testicular level, and obviously not via a receptor-mediated mechanism. Compounds which would potentially fit this category would be eurycoma as well as those that directly and potently activate adenylate cyclase, bypassing the LH/hCG receptor on the leydig cells. Sclaremax would be an example.

The Bottom Line

As men age, we tend to experience a disruption in normal homeostatic function. Specifically, itâ??s likely that both an impairment of GnRH secretion (or access to the anterior pituitary) and decreased testicular steroidogenesis contribute to the decrease in endogenous Testosterone.

Compounds which increase testicular steroidogenesis via non-receptor-mediated mechanisms are most preferable in terms of a potential means of combating this age-related decline. (1-9)[/b]

Here is the article link:

So, sure I believe that as we age our testicles no longer respond as they did when we were younger. I think it would be great, if by shutting down natural production, we could keep the testicles sensitive to LH/hCG-because even if GnRH secretion is inhibited as we age, we could still use hCG to keep the testicles pumping out testosterone.

At what point do the leydig cells become so insensitive to LH/hCG that they will no longer respond? I have no clue, and am personally hoping it’s later rather than sooner, as during the past two and a half years I have been on far longer than I have been off.

Also, is the long recovery time worth the supposed benefits gained from keeping the testicles young? Does that make sense? I guess I’m trying to say, if it takes you a year or so to get the HPTA back up and running to normal or above normal, what has your health been like during that year or so of low testosterone?

Though, I have a hard time believing what happens in a rat will happen in a man. Perhaps if one kept HPTA shutdown duration to a minimum-and did not use excessively long cycles-he could take advantage of the supposed benefits of testicular shutdown.

I don’t know, I’m just rambling at this point. Anyone else care to comment??


#5

a lab rat (brown rat) can live for 2 years usually (up to 3). The mortablity rate for wild rate is 95% in the first year. It’s a very short life span. Does this correlate well with bipedal primates? It is hard to tell IMO.
It is a very crude method anyway. TRT/HRT is pretty simple for older guys. I think genetic manipulation is the future trend. It is far superior to any chemical “fixes”.


#6

It is something i would hope too as my using stats are very similar to yours it seems WHB, but as the rat-human trials go i do not see the results being as comparable as we’d like.

It is my opinion that the trials involving rodent subjects… AREN’T supposed to be directly related to how humans respond. It is simply because we as ‘hardcore’ BB’s are so quick to find the next best thing, the next new product or the newest research that shows x or y increases in anabolism, we look to rodent research and try to apply that directly to humans.

Look at IGF-1 LR3. In rodents it was a wonder miracle drug. Absolutely amazing… in human trials - not the case. BUT we use it anyway! (for that example IGF DOES have a decent anabolic effect IME, but if used correctly - low dose, frequent but short cycles, w/GH and AAS)…

IMO :wink:


#7

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#8

That’s true talk for sure BBB. I agree that a lack of results, poor recovery, and a number of other reasons is what attracted me to AAS. Also, the realization of what it did for me-even when used at low doses-is the reason I have chosen to be on more often than not.