Is this the Holy Grail of HRT/Anti-aging?

In my recent interview with Author L Rea, I asked about formestane and the alleged suppressive effects of its metabolites.

Formestane potentiates "IGF-1 release and excellent ability to decrease estogen while stimulating HPTA activity. Some seem to feel that it readily converts to testosterone-OH and therefore has HPTA suppressive effects itself. This is not so.

"First, it would do so by way of the 17bhsd enzyme - the same one that was supposed to turn all of the gyno causing oral androstenedione into "amazing amounts of testosterone". And how did that one work out? Pretty poor as there is a very unlikely potential and even less available 17bhsd to do the deed."

FYI, he does however say his personal favorite is a product that includes the trademarked Dianestrozole.
 
Anitestrogens and blood lipids

Another question of relevance here...

We know that certain AAS can adversely affect LDL and HDL cholesterol. How do antiestrogens affect blood lipids? Can they exacerbate the negative effects by lowering estrogen too much?

ALR: That more depends upon the products and drugs used. A correctly formulated supplemental product for estrogen control would take this into account and aid HDL/LDL ratios favorably.

As to drugs I have noted, the long-term use of anastrozole often leads to very low HDL (the good cholesterol). This can usually be corrected or off-set by co-commitant use of tamoxifen.
 
good news admin...I have been taking it (via IM) for 3 weeks now and along with Avena Sativa and some other goodies...I feel great! Strength gains stayed, testicles are full, sex drive is still great....my PCT was a great success!
 
Has formestane been shown to alter IGF-1 levels in MALES? Or is this another example of studies performed on females being extrapolated to males?

It is not FDA-approved, to my knowledge, so I cannot use it. I am going to begin exploring using Aromasin (exemestane), though, as it is legal in this country.

I would like to know what the proposed mechanism would be for this particular medication to unfavorably affect the lipid profile, while another of its same class does not (i.e. Arimidex--although the latter is a competitive, rather than irreversible, inhibitor). It is my understanding that as long as E levels are not driven too low this does not happen.
 
The reason androstenedione elevates E instead of T is because of the tremenodus preference of it as substrate for Aromatase.
 
SWALE said:
DHEA will not boost T levels in males (but will for females). It will elevate E, though.

I discussed the keto-DHEA with a chemist recently, who told me it does not act as straight DHEA does. All I have is his professional opinion to go on.
It's my understanding that keto-DHEA does not convert to T OR E. keto-DHEA supposedly works by competing with cortisol at the receptors thereby reducing the negative, stress-induced effects of cortisol.
 
I tried keto-DHEA a few months ago. It indeed killed my appetite. I stopped it, though, because I then had only breakthrough hunger, for sweets. There was no desire whatsoever for my usual diet of fresh veggies and so forth.
 

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