actevaTE (nettle root extract) to prevent hair loss?

sundevil04

Member
"Nettle extracts also inhibit enzymes such as 5 alpha reductase that cause testosterone to convert to DHT. It is the DHT metabolite of testosterone that is known to cause benign prostate enlargement, excess facial hair and hair loss at the top of the head."

I picked this up from another site is this saying that it can increase free test AND help hair loss?
 
While the nettle may arrest benign prostate enlargement it might not be due to dht inhibition. There are a number of chemicals in nettle and some act as 5AR inhibitors while I believe one acts as an anti-androgen competively binding to the AR. Perhaps divanil possess this property as well, if it binds to SHBG why not the AR as well?

I ran Act alone and noticed some gyno flare-up but absolutely no prostate problems. Reason being is divanil prevents the R-SHBG cell binding whereby E then binds to the complex causing bph. This pathway is likely more responsible for bph than dht.
 
ersatz said:
While the nettle may arrest benign prostate enlargement it might not be due to dht inhibition. There are a number of chemicals in nettle and some act as 5AR inhibitors while I believe one acts as an anti-androgen competively binding to the AR. Perhaps divanil possess this property as well, if it binds to SHBG why not the AR as well?
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Any idea which lignan(s) inhibit 5AR and which act as anti-androgen(s)?
 
If it binds to SHBG, then it is also freeing more DHT into your system (it will "activate" more DHT than it activates "T"). So it's possible this could be a wash.

This was discussed a little when activate was first released.
 
rrgg said:
If it binds to SHBG, then it is also freeing more DHT into your system (it will "activate" more DHT than it activates "T"). So it's possible this could be a wash.

This was discussed a little when activate was first released.
Click to expand...

While ActivaTe will free up DHT and estradiol it won't be nearly to the degree that Testosterone is released. Very small amounts of DHT and Estradiol occur in the system relative to T and subsequently bound to SHBG. Most of the DHT and E is formed through aromatization, I believe.

It won't activate more DHT than T simply because there isn't more dht than T, not by a long shot. Also DHT has a binding affinity 1.2 times higher than T. (J Steroid Biochem. 1986 Feb;24(2):549-55. The temperature dependence of the binding of 5 alpha-dihydrotestosterone, testosterone and estradiol to the sex hormone globulin (SHBG) of human plasma.) And apparently 4 times more than E2. Thus we could expect those with the lowest affinity to be displaced first.

As for the ligans responsbile for 5AR inhibition, I've seen no specifics mentioned just lumped under beta-sitosterol or other plant sterol. As for the anti-androgens apparently whatever binds to SHBG can apparently bind to the AR. Not sure if that's necessarily true but I believe that was the rationale as one ligan may have.

What perplexes me the most is that people use this product for PCT. All indications are that messing with SHBG will prolong HPTA shutdown and thus it would be counterproductive to PCT. It appears that we would want to increase SHBG initially to stimulate endo T production adn then maybe 3 weeks into PCT use ActivaTe or simliar products.
 
Really? From reading the attached link, SHBG binds to a lot more DHT than testosterone (3.4 times as much). If ActivaTe reduces SHBG binding, then doesn't this mean when ActivaTe releases bound testosterone, it will also release 3.4 times as much DHT? I think so since the article implies androgenic alopecia can result from low SHBG.

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From table 1: SHBG equilibrium constants at 37 degree C
(K in units of 1E9/M)
DHT 5.5
Testosterone 1.6
Androstenediol 1.5
Estradiol 0.68
Estrone 0.15
DHEA 0.066
Progesterone 0.09
 
K is used to represent binding affinity, not the amount bound. It even states such in the preceding paragraph."The glycosylated heterodimer (80 to 100kDa) binds 5α-dihydrotestosterone (DHT) most tightly, followed by testosterone and estradiol."
 
I think the idea of using it for pct is to raise usable test as high as possible the first couple of weeks so you dont loose much muscle. the test levels and estrogen levels will still be so low that your test will raise. probably not as fast as it would without the nettle but your usable testosterone is preserving muscle. I taper the nettle with the most towards the 1st week then less towards the 4th week. thoughts on this?
 
wastedwhiteboy2 said:
I think the idea of using it for pct is to raise usable test as high as possible the first couple of weeks so you dont loose much muscle. the test levels and estrogen levels will still be so low that your test will raise. probably not as fast as it would without the nettle but your usable testosterone is preserving muscle. I taper the nettle with the most towards the 1st week then less towards the 4th week. thoughts on this?
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I think you're dosing it backwards. I wouldn't run it until the 3 week of PCT for numerous reasons. Your endogenous testorsterone level is non-existant so there won't be much if any T to free up during the first week(s) of PCT. Also if you use clomid or nolva as part of your PCT then SHBG production should be quite dramatic. Nandi speculated that the high SHBG levels would help clear out the exogenous steroids and estrogen thus in effect priming the HPTA to start endo T production. SHBG is necessary to clear these exogenous steroids as I believe glucuronidation can't metabolize them well. (It may have only applied to methyl test though). I've seen some posts by BigCat that also support this theory to a degree though some are apt to dismiss his comments out of disdain for him. The role of SHBG in PCT is quite debateable and one must also factor in other binding proteins like albumin but I believe it wuld be best to start Act midway through PCT.
 
ersatz- In light of that, how would you dose activaTe solo? I think Derek C. did this a few months ago.
 
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