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Im doing deca sust stack is saw palmetto ok with the deca
- Thread starter rush
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DTOX
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I'm sure I'll get flamed for this, but Saw Palmetto extract is the *last* thing you want to be taking during a cycle (or any other time for that matter) as it is an antiandrogen (though a weak one). What little effect it has is by binding (or blocking) androgens--and not just DHT but all androgens. If you're worried about your hair for fucksake get some proscar or propecia or just do deca or EQ, etc.
If you disagree you're cordially invited to do a search on saw palmetto and permixon on PubMed and read for yourself...
If you disagree you're cordially invited to do a search on saw palmetto and permixon on PubMed and read for yourself...
According to this particular study, saw palmetto exhibits neither anti-androgenic activivity nor 5 alpha reductase inhibition.
Comparison of finasteride (Proscar), a 5 alpha reductase inhibitor, and various commercial plant extracts in in vitro and in vivo 5 alpha reductase inhibition.
Rhodes L, Primka RL, Berman C, Vergult G, Gabriel M, Pierre-Malice M, Gibelin B.
Department of Biochemistry, Merck Research Laboratories, Rahway, New Jersey 07065.
Human prostate was used as a source of 5 alpha reductase. Compounds were incubated with an enzyme preparation and [3H]testosterone. [3H]-dihydrotestosterone production was measured to calculate 5 alpha reductase activity. IC50 values (ng/ml) were finasteride = 1; Permixon = 5,600; Talso = 7,000; Strogen Forte = 31,000; Prostagutt = 40,000; and Tadenan = 63,000. Bazoton and Harzol had no activity at concentrations up to 500,000 ng/ml. In castrate rats stimulated with testosterone (T) or dihydrotestosterone (DHT), finasteride, but not Permixon or Bazoton, inhibited T stimulated prostate growth, while none of the three compounds inhibited DHT stimulated growth. These results demonstrate that finasteride inhibits 5 alpha reductase, while Permixon and Bazoton have neither anti-androgen nor 5 alpha reductase inhibitory activity. In addition, in a 7 day human clinical trial, finasteride, but not Permixon or placebo, decreased serum DHT in men, further confirming the lack of 5 alpha reductase inhibition by Permixon. Finasteride and the plant extracts listed above do not inhibit the binding of DHT to the rat prostatic androgen receptor (concentrations to 100 micrograms/ml). Based on these results, it is unlikely that these plant extracts would shrink the prostate by inhibiting androgen action or 5 alpha reductase.
Comparison of finasteride (Proscar), a 5 alpha reductase inhibitor, and various commercial plant extracts in in vitro and in vivo 5 alpha reductase inhibition.
Rhodes L, Primka RL, Berman C, Vergult G, Gabriel M, Pierre-Malice M, Gibelin B.
Department of Biochemistry, Merck Research Laboratories, Rahway, New Jersey 07065.
Human prostate was used as a source of 5 alpha reductase. Compounds were incubated with an enzyme preparation and [3H]testosterone. [3H]-dihydrotestosterone production was measured to calculate 5 alpha reductase activity. IC50 values (ng/ml) were finasteride = 1; Permixon = 5,600; Talso = 7,000; Strogen Forte = 31,000; Prostagutt = 40,000; and Tadenan = 63,000. Bazoton and Harzol had no activity at concentrations up to 500,000 ng/ml. In castrate rats stimulated with testosterone (T) or dihydrotestosterone (DHT), finasteride, but not Permixon or Bazoton, inhibited T stimulated prostate growth, while none of the three compounds inhibited DHT stimulated growth. These results demonstrate that finasteride inhibits 5 alpha reductase, while Permixon and Bazoton have neither anti-androgen nor 5 alpha reductase inhibitory activity. In addition, in a 7 day human clinical trial, finasteride, but not Permixon or placebo, decreased serum DHT in men, further confirming the lack of 5 alpha reductase inhibition by Permixon. Finasteride and the plant extracts listed above do not inhibit the binding of DHT to the rat prostatic androgen receptor (concentrations to 100 micrograms/ml). Based on these results, it is unlikely that these plant extracts would shrink the prostate by inhibiting androgen action or 5 alpha reductase.
Suspension
New member
DTOX said:Either way it's crap.
I could cut & paste other abstracts...but my point wasn't about what saw palmetto does or doesn't do but it's uselessness.
I'm not sure why one would even be concerned if they're just doing deca...
Hey dumbass, read this:
"The liposterolic (fat-soluble) extract of saw palmetto provides fatty acids, sterols, and esters. The extract is thought to reduce the amount of dihydrotesterone (an active form of testosterone) LOCALLY in the part of the prostate surrounding the urethra.1 Saw palmetto is not thought to inhibit production of this form of testosterone elsewhere in the body.2 Saw palmetto also inhibits the actions of inflammatory substances that may contribute to benign prostatic hyperplasia (BPH). Contrary to some opinions, saw palmetto does not exert an estrogenic effect in men’s bodies."
Suspension
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I wouldnt say its useless! It may not prevent hairloss, but it is good for other things.
S
Stew Meat
Guest
Suspension said:
NEVER take saw palmetto w/ deca. Deca will convert to DHN wich has low androgenic activity outside of muscle tissue. However, if you block deca's conversion to DHN, it will become heavily androgenic in prostate and scalp... I know how it behaves in the scalp and I'm only assuming that it behaves the same way in the scalp. It must alpha reduce or it is very hard on tissues other than the muscle cells.
-Stew
Suspension
New member
Stew Meat said:
Thats odd, I took Saw Palmetto ED during my first cycle of Deca/Sust/Dbol. I didnt experience any hairloss. And as a matter of fact, I was taking up to 6 capsules of standardized saw palmetto ED.
