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DHT blocker on test


jimmybro1

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What effects would this have? Would it influence the effectiveness of the cycle. What would be required to get DHT levels at bay throughout the cycle at a particular dose (I.e. 500mg/wk).

Seems to be a few bits and pieces on the forums on line but I was wondering what experienced peoples thoughts were here.

During post cycle would the DHT blocker need to be continued?

I realize DHT blocker like fin have side effects that effect the sex drive I have a friend that's been on it for a year and doesn't notice any effects. After all DHT is responable for your sexual organs!

Also running a DHT along side test will help minimize risk of prostate enlargement also.

NOTE: typed on phone.

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I think finisteride has a therpetic window for blocking DHT at 1mg (dont quote me on this just my very basic understanding) and if you start to run more than that its highly diminishable as to any benefit (i get gyno if i run over 1.5mg/day) . i run 1.25mg and that seems to be the sweet spot. Ive noticed my cycles arent as great as they used to be ( i only run <1ml at anytime though) seems to have the biggest impact on strength and mass to lesser extent.

There is no point taking fina just for the duration of a cycle as it takes 6 months to a year to start working effectivley. If you're going to use it, you start and you stay on. Any shedding from using gear is either temporary and nothing to worry about or is the result of a speed up genetic MPB process. So you're in two camps 1. you dont need to worry about it will grow back or, 2. You're going bald reguardless and gear will speed that process up but not make you bald in the first place (get on and stay on).

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500mg test per week on its own is a stupid cycle. no idea why anyone would recomend it. heres your cycle:

 

250mg test (e2d)

200mg deca/npp (e2d)

Peptides (3x/day)

oral(s) (training days)

AI/SERM (only take if get bloat/gyno etc while symptoms present)

 

thats a proper cycle that will actually build muscle and get you stronger and keep you lean. i can elaborate on peptides on fb coz cbf sharing such here. stuff in bold most crucial. npp/deca could swap for tren but IMO nandrolone suit you better

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500mg test per week on its own is a stupid cycle. no idea why anyone would recomend it. heres your cycle:

 

250mg test (e2d)

200mg deca/npp (e2d)

Peptides (3x/day)

oral(s) (training days)

AI/SERM (only take if get bloat/gyno etc while symptoms present)

 

thats a proper cycle that will actually build muscle and get you stronger and keep you lean. i can elaborate on peptides on fb coz cbf sharing such here. stuff in bold most crucial. npp/deca could swap for tren but IMO nandrolone suit you better

Nandrolone is terrible for hair loss so ount that one out straight away. Nothing wrong with 500mg test!

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Do you stay on test or come off cycle?

If not running test notice much of an impact on strength/hypertrophy ?

How long have you been on fin ?

Stay on most of the time, come off now and then for 6 weeks at a time. i havent been training properly for the last couple years, so it more to prevent me from withering away too rapidly. I wouldnt call it a 'cycle' i barely eat 2 meals a day and only hit the gym once/twice a week most of the time (looking to step it up for summer a bit though).

Training natty is joke imo, id never bother, besides whats 3/4-1ml a week in the scheme of things?

Been a bit inconsistent but year or so.

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What effects would this have? Would it influence the effectiveness of the cycle. What would be required to get DHT levels at bay throughout the cycle at a particular dose (I.e. 500mg/wk).

Seems to be a few bits and pieces on the forums on line but I was wondering what experienced peoples thoughts were here.

During post cycle would the DHT blocker need to be continued?

I realize DHT blocker like fin have side effects that effect the sex drive I have a friend that's been on it for a year and doesn't notice any effects. After all DHT is responable for your sexual organs!

Also running a DHT along side test will help minimize risk of prostate enlargement also.

NOTE: typed on phone.

Why do you wish to knockout DHT.?

No DHT = posibility of gyno..

Prostrate issues = Raloxifene 60mg/day

For health reasons avoid drugs like finasteride, & dutasteride.. Seriously. Hair loss is not life-threatening, while these drugs are teratogenic poisons

 

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i run 1.25mg and that seems to be the sweet spot.

Is that an off-cycle dose, TWL? Do you increase it on-cycle?

I'm on much the same... 2.5mg 3x a week. If I do a cycle, I presume I would increase it a bit? Or maybe I'd just keep it the same until I see an increase is needed.

There is no point taking fina just for the duration of a cycle as it takes 6 months to a year to start working effectivley

Maybe it depends how thin your hair has become, but I reckon I was seeing less scalp at 6-8 weeks. Certainly less than 6 months - I haven't been on it that long yet.

i get gyno if i run over 1.5mg/day

I definitely noticed more water in my hand and ankles on 2.5mg/day.

Not sure about its effect on strength... I did start feeling weaker, and this was in the back of my mind (I chose to ignore it!) - but it could equally just be lack of sleep too.

 

 

these drugs are teratogenic poisons

I hope this doesn't sound flippant, Daz... but as a guy I don't plan on becoming pregnant any time soon!

Seriously though, while I agree you don't want to suppress DHT entirely, it seems that for those with higher DHT levels, lowering it may not be such a bad thing? Especially if you're on a cycle, where a DHT blocker like fina can (I think) counter some of the testosterone-induced sides like prostate enlargement?

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Maybe consider anabolics that don't convert to DHT so easily or arnt so androgenic.

EQ is a good one, doesn't convert to estrogen or dht as easily as test. 

 

Some copy paste :

Not all steroids can be converted to dihydrotestosterone. Test is converted by action of 5-alpha reductase, an enzyme that reduces the 4,5-double bond of test to make dihydrotestosterone. Not all steroids even have a 4,5-double bond to be reduced. Primo does not have such a double bond and can not be reduced to a dihydrotestosterone derivative. Equipoise - boldenone undecylenate - does have a 4,5-double bond that can be reduced but it also hs a 1,2 double bond which can not be reduced so 5-AR will convert Equipoise - boldenone undecylenate - into 1-test to some degree but Equipoise - boldenone undecylenate - can not be reduced all the way down to dihydrotestosterone. 
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Maybe consider anabolics that don't convert to DHT so easily or arnt so androgenic.

EQ is a good one, doesn't convert to estrogen or dht as easily as test. 

 

Some copy paste :

Not all steroids can be converted to dihydrotestosterone. Test is converted by action of 5-alpha reductase, an enzyme that reduces the 4,5-double bond of test to make dihydrotestosterone. Not all steroids even have a 4,5-double bond to be reduced. Primo does not have such a double bond and can not be reduced to a dihydrotestosterone derivative. Equipoise - boldenone undecylenate - does have a 4,5-double bond that can be reduced but it also hs a 1,2 double bond which can not be reduced so 5-AR will convert Equipoise - boldenone undecylenate - into 1-test to some degree but Equipoise - boldenone undecylenate - can not be reduced all the way down to dihydrotestosterone. 

 

 

The introduction of extra substituents like a 7a-methyl group in bolasterone and MENT may hamper the action of 5AR and prevent reduction. Methyl groups at the bottom side of the molecule hinder the approach of the co-enzyme that has to deliver the H-atom there.

Also the introduction of a Cl-atom at C4, as in clostebol, makes the reduction of the D4 double bond more difficult. This is not only the result of steric hindrance but the Cl-atom also has a stabilising interaction with the double bond.

The introduction of a D1-double bond, as in dianabol, is also detrimental for reduction of the D4-double bond. The reason for this effect is not really clear. It may be that the change in shape of the molecule may lead to a misfit of the molecule in the reducing enzyme 5AR. An other reason may be that the activating effect of the carbonyl group now has to be divided over two double bonds. For this reason the activation may be insufficient for reduction of the D4-double bond.

 
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Unsure as to why you would wish to knock out DHT, when it can be shown to contribute to skeletal muscle hypertrophy..

 

Skeletal muscle growth and fiber composition in mice are regulated through the transcription factors STAT5a/b: linking growth hormone to the androgen receptor, Peter Klover, September 2009 The FASEB Journal vol. 23 no. 9 3140-3148

 

Androgens testosterone and dihydroxytestosterone in males send an additional growth signal through the AR, controlling male-specific skeletal muscle growth...

 

Local autocrine/paracrine IGF-1 is what is important for muscle growth. In other words IGF-1 made in muscle & used there, not the systemic IGF-1 circulating from the liver is what contributes to muscle growth.


- GH that acts in muscle promotes Stat5a/b signaling.


- Stat5a/b signaling acts to promote BOTH IGF-1 expression and Androgen receptor expression in skeletal muscle.


- The enhanced Androgen Receptor promote muscle growth when androgens bind.

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  • 3 weeks later...

 

 

Maybe consider anabolics that don't convert to DHT so easily or arnt so androgenic.

EQ is a good one, doesn't convert to estrogen or dht as easily as test. 

 

Some copy paste :

Not all steroids can be converted to dihydrotestosterone. Test is converted by action of 5-alpha reductase, an enzyme that reduces the 4,5-double bond of test to make dihydrotestosterone. Not all steroids even have a 4,5-double bond to be reduced. Primo does not have such a double bond and can not be reduced to a dihydrotestosterone derivative. Equipoise - boldenone undecylenate - does have a 4,5-double bond that can be reduced but it also hs a 1,2 double bond which can not be reduced so 5-AR will convert Equipoise - boldenone undecylenate - into 1-test to some degree but Equipoise - boldenone undecylenate - can not be reduced all the way down to dihydrotestosterone. 

 

 

 

The introduction of extra substituents like a 7a-methyl group in bolasterone and MENT may hamper the action of 5AR and prevent reduction. Methyl groups at the bottom side of the molecule hinder the approach of the co-enzyme that has to deliver the H-atom there.

Also the introduction of a Cl-atom at C4, as in clostebol, makes the reduction of the D4 double bond more difficult. This is not only the result of steric hindrance but the Cl-atom also has a stabilising interaction with the double bond.

The introduction of a D1-double bond, as in dianabol, is also detrimental for reduction of the D4-double bond. The reason for this effect is not really clear. It may be that the change in shape of the molecule may lead to a misfit of the molecule in the reducing enzyme 5AR. An other reason may be that the activating effect of the carbonyl group now has to be divided over two double bonds. For this reason the activation may be insufficient for reduction of the D4-double bond.

 

in english daz? lol

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Maybe consider anabolics that don't convert to DHT so easily or arnt so androgenic.

EQ is a good one, doesn't convert to estrogen or dht as easily as test. 

 

Some copy paste :

Not all steroids can be converted to dihydrotestosterone. Test is converted by action of 5-alpha reductase, an enzyme that reduces the 4,5-double bond of test to make dihydrotestosterone. Not all steroids even have a 4,5-double bond to be reduced. Primo does not have such a double bond and can not be reduced to a dihydrotestosterone derivative. Equipoise - boldenone undecylenate - does have a 4,5-double bond that can be reduced but it also hs a 1,2 double bond which can not be reduced so 5-AR will convert Equipoise - boldenone undecylenate - into 1-test to some degree but Equipoise - boldenone undecylenate - can not be reduced all the way down to dihydrotestosterone. 

 

 

 

The introduction of extra substituents like a 7a-methyl group in bolasterone and MENT may hamper the action of 5AR and prevent reduction. Methyl groups at the bottom side of the molecule hinder the approach of the co-enzyme that has to deliver the H-atom there.

Also the introduction of a Cl-atom at C4, as in clostebol, makes the reduction of the D4 double bond more difficult. This is not only the result of steric hindrance but the Cl-atom also has a stabilising interaction with the double bond.

The introduction of a D1-double bond, as in dianabol, is also detrimental for reduction of the D4-double bond. The reason for this effect is not really clear. It may be that the change in shape of the molecule may lead to a misfit of the molecule in the reducing enzyme 5AR. Another reason may be that the activating effect of the carbonyl group now has to be divided over two double bonds. For this reason the activation may be insufficient for reduction of the D4-double bond.

 

in english daz? lol

 

 

I was trying to explain why DHT conversion via 5-alpha reduction is difficult or impossible in some modified testosterones due to the arrangement of carbon/chlorine atoms, .... 

Sorry if you were confused...

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