This is a bump of TC's article "Estrogen's Dirty Little Secret" from a few years ago. The original thread was locked, hence the re-post. Really good article. I don't know if this will generate much discussion, but hope it does. Any updates?
Pretty lame that it doesn't pop up in the T-Nation search window, though the shortcomings of that function is hardly new information.
I don't understand TC's Finasteride comment towards the end. He is taking some sort of testosterone booster, but in order to counteract negative effects on his prostate and hairline, he takes Finasteride, which lowers T?
An unrelated post didn't show up again...
Anyway, Finasteride (I'm pretty sure) only lowers DHT, not Test. DHT is highly anabolic though, so your point is right, that it would be bad for muscle gain. Unfortunately lowering DHT is also how it keeps hair from falling out.
DHT is a strong androgen. Binds to the androgen receptor with greater affinity than testosterone. WHy do you say it's highly anabolic?
Oops. I goofed. You were just lurking in this thread, biding your time before someone made a goof about something like that, weren't you!? Haha, j/k. Yeah you're totally right though
I seem to recall that DHT is not very active in skeletal muscle, however, because 5-alpha reductase isn't very prominent there and also, what little DHT is made is supposedly enzymatically inactivated by another enzyme in skeletal muscle.
Any truth to this? Because if so then it seems 5-AR inhibitors would not seem to affect muscle growth very much (at least on paper) since there is little DHT in muscle anyways.
That is mostly true (thanks to Bonez for refreshing my memory), however, androgenic substances like DHT have their place. Maybe Bonez or someone with more experience can elaborate.
Right, my point wasn't that androgenic substances aren't of use, they very much are, but rather, DHT, or more specifically, endogenous DHT shouldn't really play a large part in muscle mass because its concentrations in skeletal muscle are normally too low to make much of a difference (again, in theory, I don't know how true that actually is.)
Or I guess my ACTUAL point was, finasteride-induced reductions in DHT shouldn't have much, if any, negative effect on building muscle if the above is true.
But yes BONEZ should drop some knowledge bombs for those of us too lazy to hunt down this crap at the moment
So what would the downside of finasteride-induced lower DHT be? Reduced libido?
So what would the result of finasteride-induced lower DHT be? Reduced libido?
Yes, among other things, since 5-AR is in the nervous system, genitals, skin - DHT being heavily concentrated in the brain and libido being a complicated neuroendocrine relationship, also CNS issues probably hinder strength and nervous system efficiency - so while direct muscle anabolism is probably largely unaffected, DHT has a lot of other positive roles.
I'm having issues understanding this. Could somebody shed some light?
Sex hormone binding globulin is regarded as one of man's big bugaboos.
Here's why: In normal men, only about 2% of our Testosterone is "free," or unbound to carrier proteins. That means that presumably, only 2% is free to be ferried into cells to make muscle grow (among other things). About 54% is bound to albumin and other proteins, and 44% is bound to Sex Hormone Binding Globulin, or SHBG, which is synthesized by the liver.
For years, strength athletes have been trying to figure out how to reduce the amount of SHBG so that more free Testosterone was available for all the good stuff, like muscle growth.
However, as studies that have been largely ignored by the strength community have revealed, it seems that we might all be full of hooey.
For one thing, it now seems that red blood cells function as carriers of sex hormones in the blood stream, and in fact may be responsible for as much as 15% of sex hormone delivery to target tissues.(7) What happens is that dissociation of this protein-bound hormone can occur within a capillary bed, meaning that it's not just the "free stuff" that's working.
The amount of hormone that can be carried depends on capillary transit time, half time of dissociation, amount of hormone bound to various carrier proteins, and permeability of cell membrane.
That means that these binding proteins in circulation act as kind of a steroid bank. In fact, it's a lot like how hemoglobin regulates the amount of oxygen in each tissue.
(This may be why the free T levels of strength athletes always seem to come up quite low on blood tests. Obviously, they're functioning just fine, but judging by their levels of free T, you'd think they were Girl Scouts.)
Just curious because my Free test levels are rock bottom as well.
Is that the source? Interesting and seems logical. Vintage studies rock.
If I read that right (correct me if not) 5-15% would be tied in the red blood cells as the "Steroid bank".
That doesn't seem enough to bring low Free testosterone numbers in strength athletes does it?
Are you sure they really are significantly lower? I only found one study that said something like that when I entered strength athlete free testosterone into pubmed.
I interpreted it as "15-30% of the hormones in the blood are in RBCs, but they only take care of 5-15% of the hormone delivery". Couldn't read more than the abstract though.
But since this study looked at blood with a pH of 7.2, I wouldn't care too much about the exact numbers as proteins often stop binding things when the pH changes.
Bring on the Rez-V !