[Jay Black]

Out of curiosity, since these two compounds are the two best known to treat gyno without surgery, if one was able to source both of them, would running them together be more effective than either alone?

[D Sade]

Out of curiosity, since these two compounds are the two best known to treat gyno without surgery, if one was able to source both of them, would running them together be more effective than either alone?

In a locallized carrier (GEl #3) DHT applied on chest would be effective. No reason to inject Epi, though.

[Kimbo]

In a locallized carrier (GEl #3) DHT applied on chest would be effective. No reason to inject Epi, though.

Are you saying that epi can be taken orally, or are you saying it would be overkill on top of the DHT?

[D Sade]

Are you saying that epi can be taken orally, or are you saying it would be overkill on top of the DHT?

Epi is methylated and designed to be taken orally. I think oral Epi plus localized DHT applied to nipple region would be a kickass combo to reduce symptoms of gyno/pseudo-gyno.

I found the same results using 3-aa powder in gel # 3.

[Kimbo]

Epi is methylated and designed to be taken orally. I think oral Epi plus localized DHT applied to nipple region would be a kickass combo to reduce symptoms of gyno/pseudo-gyno.

I found the same results using 3-aa powder in gel # 3.

I think by "epi" he was referring to epitiostanol (non-methylated version).

I tried using 3-AA back in the day - didn't do much for me, but I might not have used enough or used it for long enough.

[Jakeshorts]

I think he meant the unmethylated version that's actually meant to be injected.

[Jay Black]

Epi is methylated and designed to be taken orally. I think oral Epi plus localized DHT applied to nipple region would be a kickass combo to reduce symptoms of gyno/pseudo-gyno.

I found the same results using 3-aa powder in gel # 3.

I was referring to actual Epitiostanol, not making an injectable out of your product Since the studies were done with injectable Epitiostanol, 20mg per week for 5-8 weeks, I'm going to assume that it would be the superior method because methylation can change a compound's nature, correct? I'm assuming that's why I had a negative reaction to Havoc at 40mg ED (gyno flair up, worse than ever); but people are seeing reduction in gyno at 20mg ED...so it's a strange compound, IMO.

[D Sade]

Gotcha...My mistake. You don't see too much of the unmethylated raw around, which is why I just FIGGered.

[Kimbo]

Does anyone have any numbers from a blood test for the estrogen levels post-Havoc vs. pre-Havoc?

[dashforce]

I just finished a 2-week havoc cycle, started at 2 ED and ramped up to 4-5 for the alst couple days.

Nipples are sore -- but it feels like skin abrasion from the lipoderm more than anything.

Started topical DHT the day I stopped the havoc (~3 days ago), and my libido has never been lower. Don't know what the fuck is going on, can't hardly get an erection and can't keep one for the life of me.

[captainbicept]

I use MDHT when I am on a cycle. I t is a good harderner, and an excellent pre-workout supplement, to help add intensity to your workouts.
However, I would be interested to know how the DHT effects your gyno. Before and after pics would be cool.

[Jay Black]

I just finished a 2-week havoc cycle, started at 2 ED and ramped up to 4-5 for the alst couple days.

Nipples are sore -- but it feels like skin abrasion from the lipoderm more than anything.

Started topical DHT the day I stopped the havoc (~3 days ago), and my libido has never been lower. Don't know what the fuck is going on, can't hardly get an erection and can't keep one for the life of me.

Are you applying the topical DHT and the Lipoderm to your chest???

[dashforce]

There's a log -- search for dashforce vs gyno round 2

[Jay Black]

[avantgarde]

Dashforce I belive DHT lowers estrogen and some E2 is necessary for libido. If your endogenous test is lowered post HAVOC you got very little substrate (test) for aromatase to convert to estrogen and topical DHT might slash whatevers left to zero.

Just a guess , no way to know without the labs.

[Kimbo]

Dashforce I belive DHT lowers estrogen and some E2 is necessary for libido. If your endogenous test is lowered post HAVOC you got very little substrate (test) for aromatase to convert to estrogen and topical DHT might slash whatevers left to zero.

Just a guess , no way to know without the labs.

I think it depends on how much of the DHT is going systemic, doesn't it? He's using Andractim, so I'm thinking there is at least some going this route.

[Jakeshorts]

if andrictim is really exerting that kind of systemic effect within 3 days I am indeed impressed

[dashforce]

Dashforce I belive DHT lowers estrogen and some E2 is necessary for libido. If your endogenous test is lowered post HAVOC you got very little substrate (test) for aromatase to convert to estrogen and topical DHT might slash whatevers left to zero.

Just a guess , no way to know without the labs.

This is one of my theories as well. My shoulder was hurting last night, as it often does with either low carb or low estrogen (AI/havoc).
In addition to libido, my mood and energy sucks today. Bad. And I have a headache. According to this little article, low estrogen may well be the issue.

Maybe I'll down a quart of soy milk and see if that helps; at least that will identify the problem.

The question is why my nipples are looking bigger, not smaller, if my E is low and DHT is high...

I think it depends on how much of the DHT is going systemic, doesn't it? He's using Andractim, so I'm thinking there is at least some going this route.

There is... normally. I looked up a study the other day on its pharmacokinetics (on a few young boys 1-8 with microphallus) and was really surprised -- in one or two, DHT SPIKED at 1 hr, another one or two at 2-3 hrs, and several had no plasma increase at all. Weird.

if andrictim is really exerting that kind of systemic effect within 3 days I am indeed impressed

Not just andractim -- remember, I purposely did a havoc cycle first to induce this type of effect (if that's really what we're seeing).

Sorry, I'll move this convo back to my thread (AAMOF, I think I'll copy this post there, too).

[Jakeshorts]

Not just andractim -- remember, I purposely did a havoc cycle first to induce this type of effect (if that's really what we're seeing).

you took havoc so you'd get puffy nipples and kill your libido? By incredible systemic effect I meant your killed libido and soreness.

[dashforce]

Well, the idea was to get shut down. So the libido part follows naturally (I didn't think it would be this bad!). The puffy nipples, I'm not sure what that's all about...

[Jay Black]

I don't understand the logic behind trying to get shutdown first...

[Jay Black]

That stuff sounds excellent!!!

[dashforce]

I don't understand the logic behind trying to get shutdown first...

Basically, it's the same logic as using all those fancy AIs and SERMS -- if I shut down my T production, then aromatization to E will go down the toilet as well. So as long as I go directly from suppressive androgen (epi) to another suppressive androgen (andractim), my androgen levels will remain high and my estrogen extremely low (so low that I have ZERO libido and my joints are killing me, although my androgen levels are probably quite high).

I used the epi to shut me down first because it's cheaper than andractim, so it should (in theory) "maximize" the anti-gyno effect.


Sounds like that stuff has all the basic ingredients that everyone's already tried a billion times -- which work in theory, usually work in recent-onset gyno (esp AAS-induced), but for some reason are ineffective for persistent pubertal gyno.

[Jakeshorts]

you have to admit though Dash that transdermal delivery is a little new, at least to our little research group.

On that note, why didn't you do havoc + adrictim at the same time?

[dashforce]

Trandermal delivery is a cool thing all on its own, but its main purpose would be either avoiding system effects (like lipoderm or possibly andractim) or avoiding hepatic metabolism to increase bioavailability (like transdermal test or andractim). Other than those two reasons, I don't see why transdermal would be better than systemic. Especially for the AI -- there's a shitload of peripheral aromatase that it won't be affecting (which the SERM should take care of, but why not just use a systemic AI in that case?)

I didn't see the advantage of Havoc + andractim simultaneously. Andractim essentially does everything we want -- it competes for aromatase (AI effects), it reportedly has effects at the estrogen receptor (again, competitively), it shuts down endegenous T to slow the rate of E formation in the first place, and it activates the androgen receptor quite potently. That's the whole package -- what could epi add? I figured my $$ was better spent using epi to "prep" my body for the andractim so the effects of low E were felt from day 1 instead of taking time to fall to low levels.

[Jakeshorts]

well a suicide inhibitor right on the nips for local inhibition sounds like a winner to your boy.

Also, I wasn't aware of havoc cause that kind of shut down. I thought it was supposed to be rather mild.

[dashforce]

Suicide inhibitor on the nips is great -- but how does it help prevent T->E conversion in other body sites? That E would be just as free to activate the "nips" receptors as it would be if converted in situ.

So at the minimum, combination of localized AI and SERM would be necessary. But if you've got a localized SERM going on, what's the use of an AI? And besides, some trains of thought seem to think that ERa activation by E2 shuts down mammary mRNA (very good for our purposes). So some level of E2 pointed in the right direction could be a good thing.

As far as havoc and shutdown -- yes, it is supposed to be quite mild. I wasn't expecting a hard-core all-out shutdown, just an edge.

[Jakeshorts]

Suicide inhibitor on the nips is great -- but how does it help prevent T->E conversion in other body sites? That E would be just as free to activate the "nips" receptors as it would be if converted in situ.

So at the minimum, combination of localized AI and SERM would be necessary. But if you've got a localized SERM going on, what's the use of an AI? And besides, some trains of thought seem to think that ERa activation by E2 shuts down mammary mRNA (very good for our purposes). So some level of E2 pointed in the right direction could be a good thing.

As far as havoc and shutdown -- yes, it is supposed to be quite mild. I wasn't expecting a hard-core all-out shutdown, just an edge.

if your killing estro receptors for good locally why would it matter if T -> E went up? Not to mention that even if it did if it's expression is seriously reduced in the local nip area it couldn't get into that dangerous elevated level (locally) that's helping create the problem in the first place.

I can't comment on use of letro as well... I think this is one of those subjects that at one point we may have to admit that we don't know exactly what's going on and fall back on brotelligence. Am I pursonally at that point? No I haven't really tried yet... But i think at one point we'll look back on this on say "why didn't we listen to the juicers?"